YM155 induces apoptosis through downregulation of specificity protein 1 and myeloid cell leukemia‐1 in human oral cancer cell lines
Identifieur interne : 001459 ( Istex/Corpus ); précédent : 001458; suivant : 001460YM155 induces apoptosis through downregulation of specificity protein 1 and myeloid cell leukemia‐1 in human oral cancer cell lines
Auteurs : Khadka Sachita ; Hyun-Ju Yu ; Jun-Won Yun ; Jeong-Sang Lee ; Sung-Dae ChoSource :
- Journal of Oral Pathology & Medicine [ 0904-2512 ] ; 2015-11.
Abstract
Background: YM155 is a small‐molecule pro‐apoptotic agent which has shown to inhibit survivin expression and induce apoptosis in various cancer cells. In this study, we investigated the function and molecular mechanism of YM155 in human oral cancer cells. Methods: The apoptotic effects and related signaling pathways of YM155 were evaluated using trypan blue exclusion assay, 4′‐6‐diamidino‐2‐phenylindole staining, Western blotting, RT‐PCR, and siRNA. Results: YM155 inhibited the growth and caused caspase‐dependent apoptosis in MC3 and HN22 cells. YM155 significantly suppressed the level of survivin protein expression through proteasome‐dependent protein degradation to confirm its survivin‐inhibiting function. YM155 reduced myeloid cell leukemia‐1 (Mcl‐1) protein, but it did not alter Mcl‐1 mRNA. It was associated with the facilitation of lysosome‐dependent protein degradation. The modifications of Mcl‐1 and survivin by YM155 were caspase‐independent manner. Treatment of MC‐3 and HN22 cells with YM155 inhibited specificity protein 1 (Sp1) and the knockdown of Sp1 by siRNA demonstrated that Mcl‐1 was regulated by Sp1 protein. Conclusions: We demonstrated the novel mechanism that YM155 causes apoptosis of human oral cancer cell lines through downregulation of Sp1 and Mcl‐1. Therefore, it may be a potential anticancer drug candidate for the treatment of oral cancer.
Url:
DOI: 10.1111/jop.12299
Links to Exploration step
ISTEX:8F4DF8D109CAD6AFD3938F4E915759780F79AD2ALe document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">YM155 induces apoptosis through downregulation of specificity protein 1 and myeloid cell leukemia‐1 in human oral cancer cell lines</title><author><name sortKey="Sachita, Khadka" sort="Sachita, Khadka" uniqKey="Sachita K" first="Khadka" last="Sachita">Khadka Sachita</name><affiliation><mods:affiliation>Department of Oral Pathology, School of Dentistry, Institute of Biodegradable Material, Institute of Oral Bioscience, Chonbuk National University, Jeonju, Korea</mods:affiliation></affiliation></author><author><name sortKey="Yu, Hyun U" sort="Yu, Hyun U" uniqKey="Yu H" first="Hyun-Ju" last="Yu">Hyun-Ju Yu</name><affiliation><mods:affiliation>Department of Oral Pathology, School of Dentistry, Institute of Biodegradable Material, Institute of Oral Bioscience, Chonbuk National University, Jeonju, Korea</mods:affiliation></affiliation></author><author><name sortKey="Yun, Jun On" sort="Yun, Jun On" uniqKey="Yun J" first="Jun-Won" last="Yun">Jun-Won Yun</name><affiliation><mods:affiliation>Department of Experimental Animal Research, Biomedical Research Institute, Seoul National University Hospital, Seoul, Korea</mods:affiliation></affiliation></author><author><name sortKey="Lee, Jeong Ang" sort="Lee, Jeong Ang" uniqKey="Lee J" first="Jeong-Sang" last="Lee">Jeong-Sang Lee</name><affiliation><mods:affiliation>Department of Health and Functional Food, College of Medical Science, Jeonju University, Jeonju, Korea</mods:affiliation></affiliation><affiliation><mods:affiliation>Correspondence: Jeong‐Sang Lee, PhD, Director of Food Industry Research Institute, Health Science Research Institute, Department of Health and Functional Food, College of Medical Science, Jeonju University, Jeonju 560‐759, Korea. Tel: 82‐63‐220‐2054, Fax: 82‐63‐270‐4027, E‐mail: and Sung‐Dae Cho, DVM, PhD, Departments of Oral Pathology, School of Dentistry and Institute of Oral Bioscience, Chonbuk National University, Jeonju 561‐756, Korea. Tel: 82‐63‐270‐4025, Fax: 82‐63‐270‐4027, E‐mail:</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: jslee11@jj.ac.krefiwdsc@chonbuk.ac.kr</mods:affiliation></affiliation></author><author><name sortKey="Cho, Sung Ae" sort="Cho, Sung Ae" uniqKey="Cho S" first="Sung-Dae" last="Cho">Sung-Dae Cho</name><affiliation><mods:affiliation>Department of Oral Pathology, School of Dentistry, Institute of Biodegradable Material, Institute of Oral Bioscience, Chonbuk National University, Jeonju, Korea</mods:affiliation></affiliation><affiliation><mods:affiliation>Correspondence: Jeong‐Sang Lee, PhD, Director of Food Industry Research Institute, Health Science Research Institute, Department of Health and Functional Food, College of Medical Science, Jeonju University, Jeonju 560‐759, Korea. Tel: 82‐63‐220‐2054, Fax: 82‐63‐270‐4027, E‐mail: and Sung‐Dae Cho, DVM, PhD, Departments of Oral Pathology, School of Dentistry and Institute of Oral Bioscience, Chonbuk National University, Jeonju 561‐756, Korea. Tel: 82‐63‐270‐4025, Fax: 82‐63‐270‐4027, E‐mail:</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: jslee11@jj.ac.krefiwdsc@chonbuk.ac.kr</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:8F4DF8D109CAD6AFD3938F4E915759780F79AD2A</idno><date when="2015" year="2015">2015</date><idno type="doi">10.1111/jop.12299</idno><idno type="url">https://api.istex.fr/ark:/67375/WNG-K8XGFKSM-V/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">001459</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">001459</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main">YM155 induces apoptosis through downregulation of specificity protein 1 and myeloid cell leukemia‐1 in human oral cancer cell lines</title><author><name sortKey="Sachita, Khadka" sort="Sachita, Khadka" uniqKey="Sachita K" first="Khadka" last="Sachita">Khadka Sachita</name><affiliation><mods:affiliation>Department of Oral Pathology, School of Dentistry, Institute of Biodegradable Material, Institute of Oral Bioscience, Chonbuk National University, Jeonju, Korea</mods:affiliation></affiliation></author><author><name sortKey="Yu, Hyun U" sort="Yu, Hyun U" uniqKey="Yu H" first="Hyun-Ju" last="Yu">Hyun-Ju Yu</name><affiliation><mods:affiliation>Department of Oral Pathology, School of Dentistry, Institute of Biodegradable Material, Institute of Oral Bioscience, Chonbuk National University, Jeonju, Korea</mods:affiliation></affiliation></author><author><name sortKey="Yun, Jun On" sort="Yun, Jun On" uniqKey="Yun J" first="Jun-Won" last="Yun">Jun-Won Yun</name><affiliation><mods:affiliation>Department of Experimental Animal Research, Biomedical Research Institute, Seoul National University Hospital, Seoul, Korea</mods:affiliation></affiliation></author><author><name sortKey="Lee, Jeong Ang" sort="Lee, Jeong Ang" uniqKey="Lee J" first="Jeong-Sang" last="Lee">Jeong-Sang Lee</name><affiliation><mods:affiliation>Department of Health and Functional Food, College of Medical Science, Jeonju University, Jeonju, Korea</mods:affiliation></affiliation><affiliation><mods:affiliation>Correspondence: Jeong‐Sang Lee, PhD, Director of Food Industry Research Institute, Health Science Research Institute, Department of Health and Functional Food, College of Medical Science, Jeonju University, Jeonju 560‐759, Korea. Tel: 82‐63‐220‐2054, Fax: 82‐63‐270‐4027, E‐mail: and Sung‐Dae Cho, DVM, PhD, Departments of Oral Pathology, School of Dentistry and Institute of Oral Bioscience, Chonbuk National University, Jeonju 561‐756, Korea. Tel: 82‐63‐270‐4025, Fax: 82‐63‐270‐4027, E‐mail:</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: jslee11@jj.ac.krefiwdsc@chonbuk.ac.kr</mods:affiliation></affiliation></author><author><name sortKey="Cho, Sung Ae" sort="Cho, Sung Ae" uniqKey="Cho S" first="Sung-Dae" last="Cho">Sung-Dae Cho</name><affiliation><mods:affiliation>Department of Oral Pathology, School of Dentistry, Institute of Biodegradable Material, Institute of Oral Bioscience, Chonbuk National University, Jeonju, Korea</mods:affiliation></affiliation><affiliation><mods:affiliation>Correspondence: Jeong‐Sang Lee, PhD, Director of Food Industry Research Institute, Health Science Research Institute, Department of Health and Functional Food, College of Medical Science, Jeonju University, Jeonju 560‐759, Korea. Tel: 82‐63‐220‐2054, Fax: 82‐63‐270‐4027, E‐mail: and Sung‐Dae Cho, DVM, PhD, Departments of Oral Pathology, School of Dentistry and Institute of Oral Bioscience, Chonbuk National University, Jeonju 561‐756, Korea. Tel: 82‐63‐270‐4025, Fax: 82‐63‐270‐4027, E‐mail:</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: jslee11@jj.ac.krefiwdsc@chonbuk.ac.kr</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Journal of Oral Pathology & Medicine</title><title level="j" type="alt">JOURNAL OF ORAL PATHOLOGY AND MEDICINE</title><idno type="ISSN">0904-2512</idno><idno type="eISSN">1600-0714</idno><imprint><biblScope unit="vol">44</biblScope><biblScope unit="issue">10</biblScope><biblScope unit="page" from="785">785</biblScope><biblScope unit="page" to="791">791</biblScope><biblScope unit="page-count">7</biblScope><date type="published" when="2015-11">2015-11</date></imprint><idno type="ISSN">0904-2512</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0904-2512</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract">Background: YM155 is a small‐molecule pro‐apoptotic agent which has shown to inhibit survivin expression and induce apoptosis in various cancer cells. In this study, we investigated the function and molecular mechanism of YM155 in human oral cancer cells. Methods: The apoptotic effects and related signaling pathways of YM155 were evaluated using trypan blue exclusion assay, 4′‐6‐diamidino‐2‐phenylindole staining, Western blotting, RT‐PCR, and siRNA. Results: YM155 inhibited the growth and caused caspase‐dependent apoptosis in MC3 and HN22 cells. YM155 significantly suppressed the level of survivin protein expression through proteasome‐dependent protein degradation to confirm its survivin‐inhibiting function. YM155 reduced myeloid cell leukemia‐1 (Mcl‐1) protein, but it did not alter Mcl‐1 mRNA. It was associated with the facilitation of lysosome‐dependent protein degradation. The modifications of Mcl‐1 and survivin by YM155 were caspase‐independent manner. Treatment of MC‐3 and HN22 cells with YM155 inhibited specificity protein 1 (Sp1) and the knockdown of Sp1 by siRNA demonstrated that Mcl‐1 was regulated by Sp1 protein. Conclusions: We demonstrated the novel mechanism that YM155 causes apoptosis of human oral cancer cell lines through downregulation of Sp1 and Mcl‐1. Therefore, it may be a potential anticancer drug candidate for the treatment of oral cancer.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Khadka Sachita</name><affiliations><json:string>Department of Oral Pathology, School of Dentistry, Institute of Biodegradable Material, Institute of Oral Bioscience, Chonbuk National University, Jeonju, Korea</json:string></affiliations></json:item><json:item><name>Hyun‐Ju Yu</name><affiliations><json:string>Department of Oral Pathology, School of Dentistry, Institute of Biodegradable Material, Institute of Oral Bioscience, Chonbuk National University, Jeonju, Korea</json:string></affiliations></json:item><json:item><name>Jun‐Won Yun</name><affiliations><json:string>Department of Experimental Animal Research, Biomedical Research Institute, Seoul National University Hospital, Seoul, Korea</json:string></affiliations></json:item><json:item><name>Jeong‐Sang Lee</name><affiliations><json:string>Department of Health and Functional Food, College of Medical Science, Jeonju University, Jeonju, Korea</json:string><json:string>Correspondence: Jeong‐Sang Lee, PhD, Director of Food Industry Research Institute, Health Science Research Institute, Department of Health and Functional Food, College of Medical Science, Jeonju University, Jeonju 560‐759, Korea. Tel: 82‐63‐220‐2054, Fax: 82‐63‐270‐4027, E‐mail: and Sung‐Dae Cho, DVM, PhD, Departments of Oral Pathology, School of Dentistry and Institute of Oral Bioscience, Chonbuk National University, Jeonju 561‐756, Korea. Tel: 82‐63‐270‐4025, Fax: 82‐63‐270‐4027, E‐mail:</json:string><json:string>E-mail: jslee11@jj.ac.krefiwdsc@chonbuk.ac.kr</json:string></affiliations></json:item><json:item><name>Sung‐Dae Cho</name><affiliations><json:string>Department of Oral Pathology, School of Dentistry, Institute of Biodegradable Material, Institute of Oral Bioscience, Chonbuk National University, Jeonju, Korea</json:string><json:string>Correspondence: Jeong‐Sang Lee, PhD, Director of Food Industry Research Institute, Health Science Research Institute, Department of Health and Functional Food, College of Medical Science, Jeonju University, Jeonju 560‐759, Korea. Tel: 82‐63‐220‐2054, Fax: 82‐63‐270‐4027, E‐mail: and Sung‐Dae Cho, DVM, PhD, Departments of Oral Pathology, School of Dentistry and Institute of Oral Bioscience, Chonbuk National University, Jeonju 561‐756, Korea. Tel: 82‐63‐270‐4025, Fax: 82‐63‐270‐4027, E‐mail:</json:string><json:string>E-mail: jslee11@jj.ac.krefiwdsc@chonbuk.ac.kr</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>apoptosis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>myeloid cell leukemia‐1</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>oral cancer</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>specificity protein 1</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>YM155</value></json:item></subject><articleId><json:string>JOP12299</json:string></articleId><arkIstex>ark:/67375/WNG-K8XGFKSM-V</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Background: YM155 is a small‐molecule pro‐apoptotic agent which has shown to inhibit survivin expression and induce apoptosis in various cancer cells. In this study, we investigated the function and molecular mechanism of YM155 in human oral cancer cells. Methods: The apoptotic effects and related signaling pathways of YM155 were evaluated using trypan blue exclusion assay, 4′‐6‐diamidino‐2‐phenylindole staining, Western blotting, RT‐PCR, and siRNA. Results: YM155 inhibited the growth and caused caspase‐dependent apoptosis in MC3 and HN22 cells. YM155 significantly suppressed the level of survivin protein expression through proteasome‐dependent protein degradation to confirm its survivin‐inhibiting function. YM155 reduced myeloid cell leukemia‐1 (Mcl‐1) protein, but it did not alter Mcl‐1 mRNA. It was associated with the facilitation of lysosome‐dependent protein degradation. The modifications of Mcl‐1 and survivin by YM155 were caspase‐independent manner. Treatment of MC‐3 and HN22 cells with YM155 inhibited specificity protein 1 (Sp1) and the knockdown of Sp1 by siRNA demonstrated that Mcl‐1 was regulated by Sp1 protein. Conclusions: We demonstrated the novel mechanism that YM155 causes apoptosis of human oral cancer cell lines through downregulation of Sp1 and Mcl‐1. Therefore, it may be a potential anticancer drug candidate for the treatment of oral cancer.</abstract><qualityIndicators><score>9.065</score><pdfWordCount>4749</pdfWordCount><pdfCharCount>29315</pdfCharCount><pdfVersion>1.6</pdfVersion><pdfPageCount>7</pdfPageCount><pdfPageSize>595.276 x 782.362 pts</pdfPageSize><pdfWordsPerPage>678</pdfWordsPerPage><pdfText>true</pdfText><refBibsNative>true</refBibsNative><abstractWordCount>193</abstractWordCount><abstractCharCount>1383</abstractCharCount><keywordCount>5</keywordCount></qualityIndicators><title>YM155 induces apoptosis through downregulation of specificity protein 1 and myeloid cell leukemia‐1 in human oral cancer cell lines</title><genre><json:string>article</json:string></genre><host><title>Journal of Oral Pathology & Medicine</title><language><json:string>unknown</json:string></language><doi><json:string>10.1111/(ISSN)1600-0714</json:string></doi><issn><json:string>0904-2512</json:string></issn><eissn><json:string>1600-0714</json:string></eissn><publisherId><json:string>JOP</json:string></publisherId><volume>44</volume><issue>10</issue><pages><first>785</first><last>791</last><total>7</total></pages><genre><json:string>journal</json:string></genre><subject><json:item><value>Original Article</value></json:item><json:item><value>Original Articles</value></json:item></subject></host><ark><json:string>ark:/67375/WNG-K8XGFKSM-V</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - pathology</json:string><json:string>2 - dentistry, oral surgery & medicine</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - clinical medicine</json:string><json:string>3 - dentistry</json:string></scienceMetrix><scopus><json:string>1 - Health Sciences</json:string><json:string>2 - Dentistry</json:string><json:string>3 - Periodontics</json:string><json:string>1 - Life Sciences</json:string><json:string>2 - Biochemistry, Genetics and Molecular Biology</json:string><json:string>3 - Cancer Research</json:string><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - Otorhinolaryngology</json:string><json:string>1 - Health Sciences</json:string><json:string>2 - Dentistry</json:string><json:string>3 - Oral Surgery</json:string><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - Pathology and Forensic Medicine</json:string></scopus><inist><json:string>1 - sciences appliquees, technologies et medecines</json:string><json:string>2 - sciences biologiques et medicales</json:string><json:string>3 - sciences medicales</json:string></inist></categories><publicationDate>2015</publicationDate><copyrightDate>2015</copyrightDate><doi><json:string>10.1111/jop.12299</json:string></doi><id>8F4DF8D109CAD6AFD3938F4E915759780F79AD2A</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-K8XGFKSM-V/fulltext.pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-K8XGFKSM-V/bundle.zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/WNG-K8XGFKSM-V/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main">YM155 induces apoptosis through downregulation of specificity protein 1 and myeloid cell leukemia‐1 in human oral cancer cell lines</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher ref="https://scientific-publisher.data.istex.fr/ark:/67375/H02-QW5Q88H5-V">Wiley Publishing Ltd</publisher><availability><licence>© 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd</licence></availability><date type="published" when="2015-11"></date></publicationStmt><notesStmt><note type="content-type" subtype="article" source="article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</note><note type="publication-type" subtype="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note></notesStmt><sourceDesc><biblStruct type="article"><analytic><title level="a" type="main">YM155 induces apoptosis through downregulation of specificity protein 1 and myeloid cell leukemia‐1 in human oral cancer cell lines</title><author xml:id="author-0000"><persName><forename type="first">Khadka</forename><surname>Sachita</surname></persName><affiliation><orgName type="division">Department of Oral Pathology</orgName>
<orgName type="division">School of Dentistry</orgName>
<orgName type="division">Institute of Biodegradable Material</orgName>
<orgName type="division">Institute of Oral Bioscience</orgName>
<orgName type="institution">Chonbuk National University</orgName>
<address><settlement>Jeonju</settlement>
<country key="KP" xml:lang="en">KOREA, DEMOCRATIC PEOPLE'S REPUBLIC
OF</country></address></affiliation></author><author xml:id="author-0001"><persName><forename type="first">Hyun‐Ju</forename><surname>Yu</surname></persName><affiliation><orgName type="division">Department of Oral Pathology</orgName>
<orgName type="division">School of Dentistry</orgName>
<orgName type="division">Institute of Biodegradable Material</orgName>
<orgName type="division">Institute of Oral Bioscience</orgName>
<orgName type="institution">Chonbuk National University</orgName>
<address><settlement>Jeonju</settlement>
<country key="KP" xml:lang="en">KOREA, DEMOCRATIC PEOPLE'S REPUBLIC
OF</country></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">Jun‐Won</forename><surname>Yun</surname></persName><affiliation><orgName type="division">Department of Experimental Animal Research</orgName>
<orgName type="division">Biomedical Research Institute</orgName>
<orgName type="institution">Seoul National University Hospital</orgName>
<address><settlement>Seoul</settlement>
<country key="KP" xml:lang="en">KOREA, DEMOCRATIC PEOPLE'S REPUBLIC
OF</country></address></affiliation></author><author xml:id="author-0003" role="corresp"><persName><forename type="first">Jeong‐Sang</forename><surname>Lee</surname></persName><affiliation><orgName type="division">Department of Health and Functional Food</orgName>
<orgName type="division">College of Medical Science</orgName>
<orgName type="institution">Jeonju University</orgName>
<address><settlement>Jeonju</settlement>
<country key="KP" xml:lang="en">KOREA, DEMOCRATIC PEOPLE'S REPUBLIC
OF</country></address></affiliation></author><author xml:id="author-0004" role="corresp"><persName><forename type="first">Sung‐Dae</forename><surname>Cho</surname></persName><affiliation><orgName type="division">Department of Oral Pathology</orgName>
<orgName type="division">School of Dentistry</orgName>
<orgName type="division">Institute of Biodegradable Material</orgName>
<orgName type="division">Institute of Oral Bioscience</orgName>
<orgName type="institution">Chonbuk National University</orgName>
<address><settlement>Jeonju</settlement>
<country key="KP" xml:lang="en">KOREA, DEMOCRATIC PEOPLE'S REPUBLIC
OF</country></address></affiliation></author><idno type="istex">8F4DF8D109CAD6AFD3938F4E915759780F79AD2A</idno><idno type="ark">ark:/67375/WNG-K8XGFKSM-V</idno><idno type="DOI">10.1111/jop.12299</idno><idno type="unit">JOP12299</idno><idno type="toTypesetVersion">file:JOP.JOP12299.pdf</idno></analytic><monogr><title level="j" type="main">Journal of Oral Pathology & Medicine</title><title level="j" type="alt">JOURNAL OF ORAL PATHOLOGY AND MEDICINE</title><idno type="pISSN">0904-2512</idno><idno type="eISSN">1600-0714</idno><idno type="book-DOI">10.1111/(ISSN)1600-0714</idno><idno type="book-part-DOI">10.1111/jop.2015.44.issue-10</idno><idno type="product">JOP</idno><imprint><biblScope unit="vol">44</biblScope><biblScope unit="issue">10</biblScope><biblScope unit="page" from="785">785</biblScope><biblScope unit="page" to="791">791</biblScope><biblScope unit="page-count">7</biblScope><date type="published" when="2015-11"></date></imprint></monogr></biblStruct></sourceDesc></fileDesc><encodingDesc><schemaRef type="ODD" url="https://xml-schema.delivery.istex.fr/tei-istex.odd"></schemaRef><appInfo><application ident="pub2tei" version="1.0.10" when="2019-12-20"><label>pub2TEI-ISTEX</label><desc>A set of style sheets for converting XML documents encoded in various scientific publisher formats into a common TEI format.
<ref target="http://www.tei-c.org/">We use TEI</ref></desc></application></appInfo></encodingDesc><profileDesc><abstract style="main" xml:id="jop12299-abs-0001"><head>Background</head><p><hi rend="fc">YM</hi>155 is a small‐molecule pro‐apoptotic agent which has shown to inhibit survivin expression and induce apoptosis in various cancer cells. In this study, we investigated the function and molecular mechanism of <hi rend="fc">YM</hi>155 in human oral cancer cells.</p><head>Methods</head><p>The apoptotic effects and related signaling pathways of <hi rend="fc">YM</hi>155 were evaluated using trypan blue exclusion assay, 4′‐6‐diamidino‐2‐phenylindole staining, Western blotting, <hi rend="fc">RT</hi>‐<hi rend="fc">PCR</hi>, and si<hi rend="fc">RNA</hi>.</p><head>Results</head><p>YM155 inhibited the growth and caused caspase‐dependent apoptosis in MC3 and HN22 cells. YM155 significantly suppressed the level of survivin protein expression through proteasome‐dependent protein degradation to confirm its survivin‐inhibiting function. YM155 reduced myeloid cell leukemia‐1 (Mcl‐1) protein, but it did not alter Mcl‐1 <hi rend="fc">mRNA</hi>. It was associated with the facilitation of lysosome‐dependent protein degradation. The modifications of Mcl‐1 and survivin by YM155 were caspase‐independent manner. Treatment of MC‐3 and HN22 cells with YM155 inhibited specificity protein 1 (Sp1) and the knockdown of Sp1 by siRNA demonstrated that Mcl‐1 was regulated by Sp1 protein.</p><head>Conclusions</head><p>We demonstrated the novel mechanism that <hi rend="fc">YM</hi>155 causes apoptosis of human oral cancer cell lines through downregulation of Sp1 and Mcl‐1. Therefore, it may be a potential anticancer drug candidate for the treatment of oral cancer.</p></abstract><textClass><keywords><term xml:id="jop12299-kwd-0001">apoptosis</term><term xml:id="jop12299-kwd-0002">myeloid cell leukemia‐1</term><term xml:id="jop12299-kwd-0003">oral cancer</term><term xml:id="jop12299-kwd-0004">specificity protein 1</term><term xml:id="jop12299-kwd-0005">YM155</term></keywords><keywords rend="articleCategory"><term>Original Article</term></keywords><keywords rend="tocHeading1"><term>Original Articles</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc><revisionDesc><change when="2019-12-20" who="#istex" xml:id="pub2tei">formatting</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-K8XGFKSM-V/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component type="serialArticle" version="2.0" xml:id="jop12299" xml:lang="en"><header><publicationMeta level="product"><doi origin="wiley" registered="yes">10.1111/(ISSN)1600-0714</doi><issn type="print">0904-2512</issn><issn type="electronic">1600-0714</issn><idGroup><id type="product" value="JOP"></id></idGroup><titleGroup><title sort="JOURNAL OF ORAL PATHOLOGY AND MEDICINE" type="main">Journal of Oral Pathology & Medicine</title><title type="short">J Oral Pathol Med</title></titleGroup></publicationMeta><publicationMeta level="part" position="100"><doi origin="wiley">10.1111/jop.2015.44.issue-10</doi><copyright ownership="publisher">Copyright © 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd</copyright><numberingGroup><numbering type="journalVolume" number="44">44</numbering><numbering type="journalIssue">10</numbering></numberingGroup><coverDate startDate="2015-11">November 2015</coverDate></publicationMeta><publicationMeta level="unit" position="40" status="forIssue" type="article"><doi>10.1111/jop.12299</doi><idGroup><id type="unit" value="JOP12299"></id></idGroup><countGroup><count number="7" type="pageTotal"></count></countGroup><titleGroup><title type="articleCategory">Original Article</title><title type="tocHeading1"><i>Original Articles</i></title></titleGroup><copyright ownership="publisher">© 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd</copyright><eventGroup><event date="2014-11-03" type="manuscriptAccepted"></event><event agent="SPS" date="2014-11-14" type="xmlCreated"></event><event type="publishedOnlineEarlyUnpaginated" date="2014-12-05"></event><event type="firstOnline" date="2014-12-05"></event><event type="publishedOnlineFinalForm" date="2015-10-28"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.6.8 mode:FullText" date="2015-10-28"></event></eventGroup><numberingGroup><numbering type="pageFirst">785</numbering><numbering type="pageLast">791</numbering></numberingGroup><correspondenceTo><lineatedText><line>Correspondence: Jeong‐Sang Lee, PhD, Director of Food Industry Research Institute, Health Science Research Institute, Department of Health and Functional Food, College of Medical Science, Jeonju University, Jeonju 560‐759, Korea. Tel: 82‐63‐220‐2054, Fax: 82‐63‐270‐4027, E‐mail: <email>jslee11@jj.ac.kr</email></line><line>and Sung‐Dae Cho, DVM, PhD, Departments of Oral Pathology, School of Dentistry and Institute of Oral Bioscience, Chonbuk National University, Jeonju 561‐756, Korea. Tel: 82‐63‐270‐4025, Fax: 82‐63‐270‐4027, </line><line>E‐mail: <email>efiwdsc@chonbuk.ac.kr</email></line></lineatedText></correspondenceTo><selfCitationGroup><citation type="self" xml:id="jop12299-cit-1001"><journalTitle>J Oral Pathol Med</journalTitle> (<pubYear year="2015">2015</pubYear>) <vol>44</vol>: <pageFirst>785</pageFirst>–<pageLast>791</pageLast></citation></selfCitationGroup><attributeValueGroup><attributeValue attribute="type" element="note" value="equal"></attributeValue></attributeValueGroup><linkGroup><link type="toTypesetVersion" href="file:JOP.JOP12299.pdf"></link></linkGroup></publicationMeta><contentMeta><titleGroup><title type="main">YM155 induces apoptosis through downregulation of specificity protein 1 and myeloid cell leukemia‐1 in human oral cancer cell lines</title><title type="shortAuthors">Sachita et al.</title></titleGroup><creators><creator affiliationRef="#jop12299-aff-0001" creatorRole="author" noteRef="#jop12299-note-0001" xml:id="jop12299-cr-0001"><personName><givenNames>Khadka</givenNames> <familyName>Sachita</familyName></personName></creator><creator affiliationRef="#jop12299-aff-0001" creatorRole="author" noteRef="#jop12299-note-0001" xml:id="jop12299-cr-0002"><personName><givenNames>Hyun‐Ju</givenNames> <familyName>Yu</familyName></personName></creator><creator affiliationRef="#jop12299-aff-0002" creatorRole="author" xml:id="jop12299-cr-0003"><personName><givenNames>Jun‐Won</givenNames> <familyName>Yun</familyName></personName></creator><creator affiliationRef="#jop12299-aff-0003" corresponding="yes" creatorRole="author" xml:id="jop12299-cr-0004"><personName><givenNames>Jeong‐Sang</givenNames> <familyName>Lee</familyName></personName></creator><creator affiliationRef="#jop12299-aff-0001" corresponding="yes" creatorRole="author" xml:id="jop12299-cr-0005"><personName><givenNames>Sung‐Dae</givenNames> <familyName>Cho</familyName></personName></creator></creators><affiliationGroup><affiliation countryCode="KP" type="organization" xml:id="jop12299-aff-0001"><orgDiv>Department of Oral Pathology</orgDiv> <orgDiv>School of Dentistry</orgDiv> <orgDiv>Institute of Biodegradable Material</orgDiv> <orgDiv>Institute of Oral Bioscience</orgDiv> <orgName>Chonbuk National University</orgName> <address><city>Jeonju</city> <country>Korea</country></address></affiliation><affiliation countryCode="KP" type="organization" xml:id="jop12299-aff-0002"><orgDiv>Department of Experimental Animal Research</orgDiv> <orgDiv>Biomedical Research Institute</orgDiv> <orgName>Seoul National University Hospital</orgName> <address><city>Seoul</city> <country>Korea</country></address></affiliation><affiliation countryCode="KP" type="organization" xml:id="jop12299-aff-0003"><orgDiv>Department of Health and Functional Food</orgDiv> <orgDiv>College of Medical Science</orgDiv> <orgName>Jeonju University</orgName> <address><city>Jeonju</city> <country>Korea</country></address></affiliation></affiliationGroup><keywordGroup type="author"><keyword xml:id="jop12299-kwd-0001">apoptosis</keyword><keyword xml:id="jop12299-kwd-0002">myeloid cell leukemia‐1</keyword><keyword xml:id="jop12299-kwd-0003">oral cancer</keyword><keyword xml:id="jop12299-kwd-0004">specificity protein 1</keyword><keyword xml:id="jop12299-kwd-0005">YM155</keyword></keywordGroup><fundingInfo><fundingAgency fundRefName="National Research Foundation of Korea" funderDoi="10.13039/501100003725">National Research Foundation of Korea (NRF)</fundingAgency><fundingNumber>2014R1A4A1005309</fundingNumber></fundingInfo><abstractGroup><abstract type="main" xml:id="jop12299-abs-0001"><section xml:id="jop12299-sec-0001"><title type="main">Background</title><p><fc>YM</fc>155 is a small‐molecule pro‐apoptotic agent which has shown to inhibit survivin expression and induce apoptosis in various cancer cells. In this study, we investigated the function and molecular mechanism of <fc>YM</fc>155 in human oral cancer cells.</p></section><section xml:id="jop12299-sec-0002"><title type="main">Methods</title><p>The apoptotic effects and related signaling pathways of <fc>YM</fc>155 were evaluated using trypan blue exclusion assay, 4′‐6‐diamidino‐2‐phenylindole staining, Western blotting, <fc>RT</fc>‐<fc>PCR</fc>, and si<fc>RNA</fc>.</p></section><section xml:id="jop12299-sec-0003"><title type="main">Results</title><p>YM155 inhibited the growth and caused caspase‐dependent apoptosis in MC3 and HN22 cells. YM155 significantly suppressed the level of survivin protein expression through proteasome‐dependent protein degradation to confirm its survivin‐inhibiting function. YM155 reduced myeloid cell leukemia‐1 (Mcl‐1) protein, but it did not alter Mcl‐1 <fc>mRNA</fc>. It was associated with the facilitation of lysosome‐dependent protein degradation. The modifications of Mcl‐1 and survivin by YM155 were caspase‐independent manner. Treatment of MC‐3 and HN22 cells with YM155 inhibited specificity protein 1 (Sp1) and the knockdown of Sp1 by siRNA demonstrated that Mcl‐1 was regulated by Sp1 protein.</p></section><section xml:id="jop12299-sec-0004"><title type="main">Conclusions</title><p>We demonstrated the novel mechanism that <fc>YM</fc>155 causes apoptosis of human oral cancer cell lines through downregulation of Sp1 and Mcl‐1. Therefore, it may be a potential anticancer drug candidate for the treatment of oral cancer.</p></section></abstract></abstractGroup></contentMeta><noteGroup xml:id="jop12299-ntgp-0001"><note type="equal" xml:id="jop12299-note-0001">These authors contributed equally to this work.</note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>YM155 induces apoptosis through downregulation of specificity protein 1 and myeloid cell leukemia‐1 in human oral cancer cell lines</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>YM155 induces apoptosis through downregulation of specificity protein 1 and myeloid cell leukemia‐1 in human oral cancer cell lines</title></titleInfo><name type="personal"><namePart type="given">Khadka</namePart><namePart type="family">Sachita</namePart><affiliation>Department of Oral Pathology, School of Dentistry, Institute of Biodegradable Material, Institute of Oral Bioscience, Chonbuk National University, Jeonju, Korea</affiliation><description>These authors contributed equally to this work.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hyun‐Ju</namePart><namePart type="family">Yu</namePart><affiliation>Department of Oral Pathology, School of Dentistry, Institute of Biodegradable Material, Institute of Oral Bioscience, Chonbuk National University, Jeonju, Korea</affiliation><description>These authors contributed equally to this work.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jun‐Won</namePart><namePart type="family">Yun</namePart><affiliation>Department of Experimental Animal Research, Biomedical Research Institute, Seoul National University Hospital, Seoul, Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jeong‐Sang</namePart><namePart type="family">Lee</namePart><affiliation>Department of Health and Functional Food, College of Medical Science, Jeonju University, Jeonju, Korea</affiliation><affiliation>Correspondence: Jeong‐Sang Lee, PhD, Director of Food Industry Research Institute, Health Science Research Institute, Department of Health and Functional Food, College of Medical Science, Jeonju University, Jeonju 560‐759, Korea. Tel: 82‐63‐220‐2054, Fax: 82‐63‐270‐4027, E‐mail: and Sung‐Dae Cho, DVM, PhD, Departments of Oral Pathology, School of Dentistry and Institute of Oral Bioscience, Chonbuk National University, Jeonju 561‐756, Korea. Tel: 82‐63‐270‐4025, Fax: 82‐63‐270‐4027, E‐mail:</affiliation><affiliation>E-mail: jslee11@jj.ac.krefiwdsc@chonbuk.ac.kr</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Sung‐Dae</namePart><namePart type="family">Cho</namePart><affiliation>Department of Oral Pathology, School of Dentistry, Institute of Biodegradable Material, Institute of Oral Bioscience, Chonbuk National University, Jeonju, Korea</affiliation><affiliation>Correspondence: Jeong‐Sang Lee, PhD, Director of Food Industry Research Institute, Health Science Research Institute, Department of Health and Functional Food, College of Medical Science, Jeonju University, Jeonju 560‐759, Korea. Tel: 82‐63‐220‐2054, Fax: 82‐63‐270‐4027, E‐mail: and Sung‐Dae Cho, DVM, PhD, Departments of Oral Pathology, School of Dentistry and Institute of Oral Bioscience, Chonbuk National University, Jeonju 561‐756, Korea. Tel: 82‐63‐270‐4025, Fax: 82‐63‐270‐4027, E‐mail:</affiliation><affiliation>E-mail: jslee11@jj.ac.krefiwdsc@chonbuk.ac.kr</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><dateIssued encoding="w3cdtf">2015-11</dateIssued><dateCreated encoding="w3cdtf">2014-11-14</dateCreated><dateValid encoding="w3cdtf">2014-11-03</dateValid><edition>J Oral Pathol Med (2015) 44: 785–791</edition><copyrightDate encoding="w3cdtf">2015</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><abstract>Background: YM155 is a small‐molecule pro‐apoptotic agent which has shown to inhibit survivin expression and induce apoptosis in various cancer cells. In this study, we investigated the function and molecular mechanism of YM155 in human oral cancer cells. Methods: The apoptotic effects and related signaling pathways of YM155 were evaluated using trypan blue exclusion assay, 4′‐6‐diamidino‐2‐phenylindole staining, Western blotting, RT‐PCR, and siRNA. Results: YM155 inhibited the growth and caused caspase‐dependent apoptosis in MC3 and HN22 cells. YM155 significantly suppressed the level of survivin protein expression through proteasome‐dependent protein degradation to confirm its survivin‐inhibiting function. YM155 reduced myeloid cell leukemia‐1 (Mcl‐1) protein, but it did not alter Mcl‐1 mRNA. It was associated with the facilitation of lysosome‐dependent protein degradation. The modifications of Mcl‐1 and survivin by YM155 were caspase‐independent manner. Treatment of MC‐3 and HN22 cells with YM155 inhibited specificity protein 1 (Sp1) and the knockdown of Sp1 by siRNA demonstrated that Mcl‐1 was regulated by Sp1 protein. Conclusions: We demonstrated the novel mechanism that YM155 causes apoptosis of human oral cancer cell lines through downregulation of Sp1 and Mcl‐1. Therefore, it may be a potential anticancer drug candidate for the treatment of oral cancer.</abstract><note type="funding">National Research Foundation of Korea (NRF) - No. 2014R1A4A1005309; </note><subject><genre>keywords</genre><topic>apoptosis</topic><topic>myeloid cell leukemia‐1</topic><topic>oral cancer</topic><topic>specificity protein 1</topic><topic>YM155</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Oral Pathology & Medicine</title></titleInfo><titleInfo type="abbreviated"><title>J Oral Pathol Med</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><subject><genre>article-category</genre><topic>Original Article</topic><topic>Original Articles</topic></subject><identifier type="ISSN">0904-2512</identifier><identifier type="eISSN">1600-0714</identifier><identifier type="DOI">10.1111/(ISSN)1600-0714</identifier><identifier type="PublisherID">JOP</identifier><part><date>2015</date><detail type="volume"><caption>vol.</caption><number>44</number></detail><detail type="issue"><caption>no.</caption><number>10</number></detail><extent unit="pages"><start>785</start><end>791</end><total>7</total></extent></part></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0001"><titleInfo><title>Global epidemiology of oral and oropharyngeal cancer</title></titleInfo><name type="personal"><namePart type="given">S</namePart><namePart type="family">Warnakulasuriya</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Warnakulasuriya S. Global epidemiology of oral and oropharyngeal cancer. Oral Oncol 2009; 45: 309–16.</note><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>45</number></detail><extent unit="pages"><start>309</start><end>16</end></extent></part><relatedItem type="host"><titleInfo><title>Oral Oncol</title></titleInfo><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>45</number></detail><extent unit="pages"><start>309</start><end>16</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0002"><titleInfo><title>Tobacco smoking, alcohol drinking, and cancer of the oral cavity and oropharynx among U.S. veterans</title></titleInfo><name type="personal"><namePart type="given">A</namePart><namePart type="family">Mashberg</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P</namePart><namePart type="family">Boffetta</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R</namePart><namePart type="family">Winkelman</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Mashberg A, Boffetta P, Winkelman R, et al. Tobacco smoking, alcohol drinking, and cancer of the oral cavity and oropharynx among U.S. veterans. Cancer 1993; 72: 1369–75.</note><part><date>1993</date><detail type="volume"><caption>vol.</caption><number>72</number></detail><extent unit="pages"><start>1369</start><end>75</end></extent></part><relatedItem type="host"><titleInfo><title>Cancer</title></titleInfo><part><date>1993</date><detail type="volume"><caption>vol.</caption><number>72</number></detail><extent unit="pages"><start>1369</start><end>75</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0003"><titleInfo><title>YM155, a novel small‐molecule survivin suppressant, induces regression of established human hormone‐refractory prostate tumor xenografts</title></titleInfo><name type="personal"><namePart type="given">T</namePart><namePart type="family">Nakahara</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Kita</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K</namePart><namePart type="family">Yamanaka</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Nakahara T, Kita A, Yamanaka K, et al. YM155, a novel small‐molecule survivin suppressant, induces regression of established human hormone‐refractory prostate tumor xenografts. Cancer Res 2007; 67: 8014–21.</note><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>67</number></detail><extent unit="pages"><start>8014</start><end>21</end></extent></part><relatedItem type="host"><titleInfo><title>Cancer Res</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>67</number></detail><extent unit="pages"><start>8014</start><end>21</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0004"><titleInfo><title>Mcl‐1 downregulation by YM155 contributes to its synergistic anti‐tumor activities with ABT‐263</title></titleInfo><name type="personal"><namePart type="given">H</namePart><namePart type="family">Tang</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H</namePart><namePart type="family">Shao</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Yu</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Tang H, Shao H, Yu C, et al. Mcl‐1 downregulation by YM155 contributes to its synergistic anti‐tumor activities with ABT‐263. Biochem Pharmacol 2011; 82: 1066–72.</note><part><date>2011</date><detail type="volume"><caption>vol.</caption><number>82</number></detail><extent unit="pages"><start>1066</start><end>72</end></extent></part><relatedItem type="host"><titleInfo><title>Biochem Pharmacol</title></titleInfo><part><date>2011</date><detail type="volume"><caption>vol.</caption><number>82</number></detail><extent unit="pages"><start>1066</start><end>72</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0005"><titleInfo><title>Survivin: a new target for anti‐cancer therapy</title></titleInfo><name type="personal"><namePart type="given">BM</namePart><namePart type="family">Ryan</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">N</namePart><namePart type="family">O'Donovan</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">MJ</namePart><namePart type="family">Duffy</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Ryan BM, O'Donovan N, Duffy MJ. Survivin: a new target for anti‐cancer therapy. Cancer Treat Rev 2009; 35: 553–62.</note><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>35</number></detail><extent unit="pages"><start>553</start><end>62</end></extent></part><relatedItem type="host"><titleInfo><title>Cancer Treat Rev</title></titleInfo><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>35</number></detail><extent unit="pages"><start>553</start><end>62</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0006"><titleInfo><title>Survivin: key regulator of mitosis and apoptosis and novel target for cancer therapeutics</title></titleInfo><name type="personal"><namePart type="given">AC</namePart><namePart type="family">Mita</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">MM</namePart><namePart type="family">Mita</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">ST</namePart><namePart type="family">Nawrocki</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Mita AC, Mita MM, Nawrocki ST, et al. Survivin: key regulator of mitosis and apoptosis and novel target for cancer therapeutics. Clin Cancer Res 2008; 14: 5000–5.</note><part><date>2008</date><detail type="volume"><caption>vol.</caption><number>14</number></detail><extent unit="pages"><start>5000</start><end>5</end></extent></part><relatedItem type="host"><titleInfo><title>Clin Cancer Res</title></titleInfo><part><date>2008</date><detail type="volume"><caption>vol.</caption><number>14</number></detail><extent unit="pages"><start>5000</start><end>5</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0007"><titleInfo><title>Survivin, cancer networks and pathway‐directed drug discovery</title></titleInfo><name type="personal"><namePart type="given">DC</namePart><namePart type="family">Altieri</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Altieri DC. Survivin, cancer networks and pathway‐directed drug discovery. Nat Rev Cancer 2008; 8: 61–70.</note><part><date>2008</date><detail type="volume"><caption>vol.</caption><number>8</number></detail><extent unit="pages"><start>61</start><end>70</end></extent></part><relatedItem type="host"><titleInfo><title>Nat Rev Cancer</title></titleInfo><part><date>2008</date><detail type="volume"><caption>vol.</caption><number>8</number></detail><extent unit="pages"><start>61</start><end>70</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0008"><titleInfo><title>Overexpression of Sp1 leads to p53‐dependent apoptosis in cancer cells</title></titleInfo><name type="personal"><namePart type="given">JY</namePart><namePart type="family">Chuang</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">CH</namePart><namePart type="family">Wu</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">MD</namePart><namePart type="family">Lai</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Chuang JY, Wu CH, Lai MD, et al. Overexpression of Sp1 leads to p53‐dependent apoptosis in cancer cells. Int J Cancer 2009; 125: 2066–76.</note><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>125</number></detail><extent unit="pages"><start>2066</start><end>76</end></extent></part><relatedItem type="host"><titleInfo><title>Int J Cancer</title></titleInfo><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>125</number></detail><extent unit="pages"><start>2066</start><end>76</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0009"><titleInfo><title>Transcription factor Sp1 regulates expression of cancer‐associated molecule CD147 in human lung cancer</title></titleInfo><name type="personal"><namePart type="given">LM</namePart><namePart type="family">Kong</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">CG</namePart><namePart type="family">Liao</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">F</namePart><namePart type="family">Fei</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Kong LM, Liao CG, Fei F, et al. Transcription factor Sp1 regulates expression of cancer‐associated molecule CD147 in human lung cancer. Cancer Sci 2010; 101: 1463–70.</note><part><date>2010</date><detail type="volume"><caption>vol.</caption><number>101</number></detail><extent unit="pages"><start>1463</start><end>70</end></extent></part><relatedItem type="host"><titleInfo><title>Cancer Sci</title></titleInfo><part><date>2010</date><detail type="volume"><caption>vol.</caption><number>101</number></detail><extent unit="pages"><start>1463</start><end>70</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0010"><titleInfo><title>Chemopreventive effect of tolfenamic acid on KB human cervical cancer cells and tumor xenograft by downregulating specificity protein 1</title></titleInfo><name type="personal"><namePart type="given">JH</namePart><namePart type="family">Shim</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JA</namePart><namePart type="family">Shin</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JY</namePart><namePart type="family">Jung</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Shim JH, Shin JA, Jung JY, et al. Chemopreventive effect of tolfenamic acid on KB human cervical cancer cells and tumor xenograft by downregulating specificity protein 1. Eur J Cancer Prev 2011; 20: 102–11.</note><part><date>2011</date><detail type="volume"><caption>vol.</caption><number>20</number></detail><extent unit="pages"><start>102</start><end>11</end></extent></part><relatedItem type="host"><titleInfo><title>Eur J Cancer Prev</title></titleInfo><part><date>2011</date><detail type="volume"><caption>vol.</caption><number>20</number></detail><extent unit="pages"><start>102</start><end>11</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0011"><titleInfo><title>In vitro apoptotic effects of methanol extracts of Dianthus chinensis and Acalypha australis L. targeting specificity protein 1 in human oral cancer cells</title></titleInfo><name type="personal"><namePart type="given">JA</namePart><namePart type="family">Shin</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JJ</namePart><namePart type="family">Kim</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">ES</namePart><namePart type="family">Choi</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Shin JA, Kim JJ, Choi ES, et al. In vitro apoptotic effects of methanol extracts of Dianthus chinensis and Acalypha australis L. targeting specificity protein 1 in human oral cancer cells. Head Neck 2013; 35: 992–8.</note><part><date>2013</date><detail type="volume"><caption>vol.</caption><number>35</number></detail><extent unit="pages"><start>992</start><end>8</end></extent></part><relatedItem type="host"><titleInfo><title>Head Neck</title></titleInfo><part><date>2013</date><detail type="volume"><caption>vol.</caption><number>35</number></detail><extent unit="pages"><start>992</start><end>8</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0012"><titleInfo><title>Apoptotic effect of tolfenamic acid in androgen receptor‐independent prostate cancer cell and xenograft tumor through specificity protein 1</title></titleInfo><name type="personal"><namePart type="given">ES</namePart><namePart type="family">Choi</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JH</namePart><namePart type="family">Shim</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JY</namePart><namePart type="family">Jung</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Choi ES, Shim JH, Jung JY, et al. Apoptotic effect of tolfenamic acid in androgen receptor‐independent prostate cancer cell and xenograft tumor through specificity protein 1. Cancer Sci 2011; 102: 742–8.</note><part><date>2011</date><detail type="volume"><caption>vol.</caption><number>102</number></detail><extent unit="pages"><start>742</start><end>8</end></extent></part><relatedItem type="host"><titleInfo><title>Cancer Sci</title></titleInfo><part><date>2011</date><detail type="volume"><caption>vol.</caption><number>102</number></detail><extent unit="pages"><start>742</start><end>8</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0013"><titleInfo><title>Bax and Bak can localize to the endoplasmic reticulum to initiate apoptosis</title></titleInfo><name type="personal"><namePart type="given">WX</namePart><namePart type="family">Zong</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Li</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">G</namePart><namePart type="family">Hatzivassiliou</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Zong WX, Li C, Hatzivassiliou G, et al. Bax and Bak can localize to the endoplasmic reticulum to initiate apoptosis. J Cell Biol 2003; 162: 59–69.</note><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>162</number></detail><extent unit="pages"><start>59</start><end>69</end></extent></part><relatedItem type="host"><titleInfo><title>J Cell Biol</title></titleInfo><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>162</number></detail><extent unit="pages"><start>59</start><end>69</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0014"><titleInfo><title>ZEB2 upregulates integrin alpha5 expression through cooperation with Sp1 to induce invasion during epithelial‐mesenchymal transition of human cancer cells</title></titleInfo><name type="personal"><namePart type="given">EH</namePart><namePart type="family">Nam</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Y</namePart><namePart type="family">Lee</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">YK</namePart><namePart type="family">Park</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Nam EH, Lee Y, Park YK, et al. ZEB2 upregulates integrin alpha5 expression through cooperation with Sp1 to induce invasion during epithelial‐mesenchymal transition of human cancer cells. Carcinogenesis 2012; 33: 563–71.</note><part><date>2012</date><detail type="volume"><caption>vol.</caption><number>33</number></detail><extent unit="pages"><start>563</start><end>71</end></extent></part><relatedItem type="host"><titleInfo><title>Carcinogenesis</title></titleInfo><part><date>2012</date><detail type="volume"><caption>vol.</caption><number>33</number></detail><extent unit="pages"><start>563</start><end>71</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0015"><titleInfo><title>Mcl‐1 is a potential therapeutic target in multiple types of cancer</title></titleInfo><name type="personal"><namePart type="given">C</namePart><namePart type="family">Akgul</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Akgul C. Mcl‐1 is a potential therapeutic target in multiple types of cancer. Cell Mol Life Sci 2009; 66: 1326–36.</note><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>66</number></detail><extent unit="pages"><start>1326</start><end>36</end></extent></part><relatedItem type="host"><titleInfo><title>Cell Mol Life Sci</title></titleInfo><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>66</number></detail><extent unit="pages"><start>1326</start><end>36</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0016"><titleInfo><title>The role of Sp1 and Sp3 in normal and cancer cell biology</title></titleInfo><name type="personal"><namePart type="given">L</namePart><namePart type="family">Li</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JR</namePart><namePart type="family">Davie</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Li L, Davie JR. The role of Sp1 and Sp3 in normal and cancer cell biology. Ann Anat 2010; 192: 275–83.</note><part><date>2010</date><detail type="volume"><caption>vol.</caption><number>192</number></detail><extent unit="pages"><start>275</start><end>83</end></extent></part><relatedItem type="host"><titleInfo><title>Ann Anat</title></titleInfo><part><date>2010</date><detail type="volume"><caption>vol.</caption><number>192</number></detail><extent unit="pages"><start>275</start><end>83</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0017"><titleInfo><title>The hallmarks of cancer</title></titleInfo><name type="personal"><namePart type="given">D</namePart><namePart type="family">Hanahan</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">RA</namePart><namePart type="family">Weinberg</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Hanahan D, Weinberg RA. The hallmarks of cancer. Cell 2000; 100: 57–70.</note><part><date>2000</date><detail type="volume"><caption>vol.</caption><number>100</number></detail><extent unit="pages"><start>57</start><end>70</end></extent></part><relatedItem type="host"><titleInfo><title>Cell</title></titleInfo><part><date>2000</date><detail type="volume"><caption>vol.</caption><number>100</number></detail><extent unit="pages"><start>57</start><end>70</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0018"><titleInfo><title>Silencing of survivin gene by small interfering RNAs produces supra‐additive growth suppression in combination with 17‐allylamino‐17‐demethoxygeldanamycin in human prostate cancer cells</title></titleInfo><name type="personal"><namePart type="given">F</namePart><namePart type="family">Paduano</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R</namePart><namePart type="family">Villa</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Pennati</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Paduano F, Villa R, Pennati M, et al. Silencing of survivin gene by small interfering RNAs produces supra‐additive growth suppression in combination with 17‐allylamino‐17‐demethoxygeldanamycin in human prostate cancer cells. Mol Cancer Ther 2006; 5: 179–86.</note><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>5</number></detail><extent unit="pages"><start>179</start><end>86</end></extent></part><relatedItem type="host"><titleInfo><title>Mol Cancer Ther</title></titleInfo><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>5</number></detail><extent unit="pages"><start>179</start><end>86</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0019"><titleInfo><title>A novel antisense oligonucleotide targeting survivin expression induces apoptosis and sensitizes lung cancer cells to chemotherapy</title></titleInfo><name type="personal"><namePart type="given">RA</namePart><namePart type="family">Olie</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">AP</namePart><namePart type="family">Simoes‐Wust</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Baumann</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Olie RA, Simoes‐Wust AP, Baumann B, et al. A novel antisense oligonucleotide targeting survivin expression induces apoptosis and sensitizes lung cancer cells to chemotherapy. Cancer Res 2000; 60: 2805–9.</note><part><date>2000</date><detail type="volume"><caption>vol.</caption><number>60</number></detail><extent unit="pages"><start>2805</start><end>9</end></extent></part><relatedItem type="host"><titleInfo><title>Cancer Res</title></titleInfo><part><date>2000</date><detail type="volume"><caption>vol.</caption><number>60</number></detail><extent unit="pages"><start>2805</start><end>9</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0020"><titleInfo><title>Induction of apoptosis in human ovarian epithelial cancer cells by antisurvivin oligonucleotides</title></titleInfo><name type="personal"><namePart type="given">X</namePart><namePart type="family">Ma</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Wang</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Zhou</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Ma X, Wang S, Zhou J, et al. Induction of apoptosis in human ovarian epithelial cancer cells by antisurvivin oligonucleotides. Oncol Rep 2005; 14: 275–9.</note><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>14</number></detail><extent unit="pages"><start>275</start><end>9</end></extent></part><relatedItem type="host"><titleInfo><title>Oncol Rep</title></titleInfo><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>14</number></detail><extent unit="pages"><start>275</start><end>9</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0021"><titleInfo><title>[Clinical significance and diagnostic value of Survivin autoantibody in non‐small cell lung cancer patients]</title></titleInfo><name type="personal"><namePart type="given">L</namePart><namePart type="family">Ma</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">W</namePart><namePart type="family">Yue</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">L</namePart><namePart type="family">Zhang</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Ma L, Yue W, Zhang L, et al. [Clinical significance and diagnostic value of Survivin autoantibody in non‐small cell lung cancer patients]. Zhongguo Fei Ai Za Zhi 2010; 13: 706–12.</note><part><date>2010</date><detail type="volume"><caption>vol.</caption><number>13</number></detail><extent unit="pages"><start>706</start><end>12</end></extent></part><relatedItem type="host"><titleInfo><title>Zhongguo Fei Ai Za Zhi</title></titleInfo><part><date>2010</date><detail type="volume"><caption>vol.</caption><number>13</number></detail><extent unit="pages"><start>706</start><end>12</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0022"><titleInfo><title>Survivin and Smac gene expressions but not livin are predictors of prognosis in non‐small cell lung cancer patients treated with adjuvant chemotherapy following surgery</title></titleInfo><name type="personal"><namePart type="given">CH</namePart><namePart type="family">Dai</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Li</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">SB</namePart><namePart type="family">Shi</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Dai CH, Li J, Shi SB, et al. Survivin and Smac gene expressions but not livin are predictors of prognosis in non‐small cell lung cancer patients treated with adjuvant chemotherapy following surgery. Jpn J Clin Oncol 2010; 40: 327–35.</note><part><date>2010</date><detail type="volume"><caption>vol.</caption><number>40</number></detail><extent unit="pages"><start>327</start><end>35</end></extent></part><relatedItem type="host"><titleInfo><title>Jpn J Clin Oncol</title></titleInfo><part><date>2010</date><detail type="volume"><caption>vol.</caption><number>40</number></detail><extent unit="pages"><start>327</start><end>35</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0023"><titleInfo><title>[Increase of BIRC5 gene expression in non‐small cell lung cancer and esophageal squamous cell carcinoma does not correlate with expression of genes SMAC/DIABLO and PML encoding its inhibitors]</title></titleInfo><name type="personal"><namePart type="given">NA</namePart><namePart type="family">Vaishlia</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">MV</namePart><namePart type="family">Zinov'eva</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">AV</namePart><namePart type="family">Sass</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Vaishlia NA, Zinov'eva MV, Sass AV, et al. [Increase of BIRC5 gene expression in non‐small cell lung cancer and esophageal squamous cell carcinoma does not correlate with expression of genes SMAC/DIABLO and PML encoding its inhibitors]. Mol Biol (Mosk) 2008; 42: 652–61.</note><part><date>2008</date><detail type="volume"><caption>vol.</caption><number>42</number></detail><extent unit="pages"><start>652</start><end>61</end></extent></part><relatedItem type="host"><titleInfo><title>Mol Biol (Mosk)</title></titleInfo><part><date>2008</date><detail type="volume"><caption>vol.</caption><number>42</number></detail><extent unit="pages"><start>652</start><end>61</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0024"><titleInfo><title>Survivin–prognostic tumor biomarker in human neoplasms–review</title></titleInfo><name type="personal"><namePart type="given">J</namePart><namePart type="family">Waligorska‐Stachura</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Jankowska</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R</namePart><namePart type="family">Wasko</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Waligorska‐Stachura J, Jankowska A, Wasko R, et al. Survivin–prognostic tumor biomarker in human neoplasms–review. Ginekol Pol 2012; 83: 537–40.</note><part><date>2012</date><detail type="volume"><caption>vol.</caption><number>83</number></detail><extent unit="pages"><start>537</start><end>40</end></extent></part><relatedItem type="host"><titleInfo><title>Ginekol Pol</title></titleInfo><part><date>2012</date><detail type="volume"><caption>vol.</caption><number>83</number></detail><extent unit="pages"><start>537</start><end>40</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0025"><titleInfo><title>Expression of the antiapoptosis gene Survivin predicts poor prognosis of stage III gastric adenocarcinoma</title></titleInfo><name type="personal"><namePart type="given">KY</namePart><namePart type="family">Song</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">CK</namePart><namePart type="family">Jung</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">WS</namePart><namePart type="family">Park</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Song KY, Jung CK, Park WS, et al. Expression of the antiapoptosis gene Survivin predicts poor prognosis of stage III gastric adenocarcinoma. Jpn J Clin Oncol 2009; 39: 290–6.</note><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>39</number></detail><extent unit="pages"><start>290</start><end>6</end></extent></part><relatedItem type="host"><titleInfo><title>Jpn J Clin Oncol</title></titleInfo><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>39</number></detail><extent unit="pages"><start>290</start><end>6</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0026"><titleInfo><title>Survivin gene levels in the peripheral blood of patients with gastric cancer independently predict survival</title></titleInfo><name type="personal"><namePart type="given">L</namePart><namePart type="family">Bertazza</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Mocellin</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Marchet</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Bertazza L, Mocellin S, Marchet A, et al. Survivin gene levels in the peripheral blood of patients with gastric cancer independently predict survival. J Transl Med 2009; 7: 111.</note><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>7</number></detail><extent unit="pages"><start>111</start></extent></part><relatedItem type="host"><titleInfo><title>J Transl Med</title></titleInfo><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>7</number></detail><extent unit="pages"><start>111</start></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0027"><titleInfo><title>Survivin expression in gastric cancer: association with histomorphological response to neoadjuvant therapy and prognosis</title></titleInfo><name type="personal"><namePart type="given">D</namePart><namePart type="family">Vallbohmer</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">U</namePart><namePart type="family">Drebber</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">PM</namePart><namePart type="family">Schneider</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Vallbohmer D, Drebber U, Schneider PM, et al. Survivin expression in gastric cancer: association with histomorphological response to neoadjuvant therapy and prognosis. J Surg Oncol 2009; 99: 409–13.</note><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>99</number></detail><extent unit="pages"><start>409</start><end>13</end></extent></part><relatedItem type="host"><titleInfo><title>J Surg Oncol</title></titleInfo><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>99</number></detail><extent unit="pages"><start>409</start><end>13</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0028"><titleInfo><title>Survivin expression in colorectal carcinomas: correlations with clinicopathological parameters and survival</title></titleInfo><name type="personal"><namePart type="given">JG</namePart><namePart type="family">Kalliakmanis</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Kouvidou</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Latoufis</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Kalliakmanis JG, Kouvidou C, Latoufis C, et al. Survivin expression in colorectal carcinomas: correlations with clinicopathological parameters and survival. Dig Dis Sci 2010; 55: 2958–64.</note><part><date>2010</date><detail type="volume"><caption>vol.</caption><number>55</number></detail><extent unit="pages"><start>2958</start><end>64</end></extent></part><relatedItem type="host"><titleInfo><title>Dig Dis Sci</title></titleInfo><part><date>2010</date><detail type="volume"><caption>vol.</caption><number>55</number></detail><extent unit="pages"><start>2958</start><end>64</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0029"><titleInfo><title>Survivin: a potential prognostic marker and chemoradiotherapeutic target for colorectal cancer</title></titleInfo><name type="personal"><namePart type="given">C</namePart><namePart type="family">Xiaoyuan</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Longbang</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">W</namePart><namePart type="family">Jinghua</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Xiaoyuan C, Longbang C, Jinghua W, et al. Survivin: a potential prognostic marker and chemoradiotherapeutic target for colorectal cancer. Ir J Med Sci 2010; 179: 327–35.</note><part><date>2010</date><detail type="volume"><caption>vol.</caption><number>179</number></detail><extent unit="pages"><start>327</start><end>35</end></extent></part><relatedItem type="host"><titleInfo><title>Ir J Med Sci</title></titleInfo><part><date>2010</date><detail type="volume"><caption>vol.</caption><number>179</number></detail><extent unit="pages"><start>327</start><end>35</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0030"><titleInfo><title>Survivin expression in colorectal adenocarcinoma using tissue microarray</title></titleInfo><name type="personal"><namePart type="given">A</namePart><namePart type="family">Abd El‐Hameed</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Abd El‐Hameed A. Survivin expression in colorectal adenocarcinoma using tissue microarray. J Egypt Natl Canc Inst 2005; 17: 42–50.</note><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>17</number></detail><extent unit="pages"><start>42</start><end>50</end></extent></part><relatedItem type="host"><titleInfo><title>J Egypt Natl Canc Inst</title></titleInfo><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>17</number></detail><extent unit="pages"><start>42</start><end>50</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0031"><titleInfo><title>Survivin expression in breast carcinoma: correlation with apoptosis and prognosis</title></titleInfo><name type="personal"><namePart type="given">A</namePart><namePart type="family">Nassar</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">D</namePart><namePart type="family">Sexton</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">G</namePart><namePart type="family">Cotsonis</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Nassar A, Sexton D, Cotsonis G, et al. Survivin expression in breast carcinoma: correlation with apoptosis and prognosis. Appl Immunohistochem Mol Morphol 2008; 16: 221–6.</note><part><date>2008</date><detail type="volume"><caption>vol.</caption><number>16</number></detail><extent unit="pages"><start>221</start><end>6</end></extent></part><relatedItem type="host"><titleInfo><title>Appl Immunohistochem Mol Morphol</title></titleInfo><part><date>2008</date><detail type="volume"><caption>vol.</caption><number>16</number></detail><extent unit="pages"><start>221</start><end>6</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0032"><titleInfo><title>High expression of Survivin, mapped to 17q25, is significantly associated with poor prognostic factors and promotes cell survival in human neuroblastoma</title></titleInfo><name type="personal"><namePart type="given">A</namePart><namePart type="family">Islam</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H</namePart><namePart type="family">Kageyama</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">N</namePart><namePart type="family">Takada</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Islam A, Kageyama H, Takada N, et al. High expression of Survivin, mapped to 17q25, is significantly associated with poor prognostic factors and promotes cell survival in human neuroblastoma. Oncogene 2000; 19: 617–23.</note><part><date>2000</date><detail type="volume"><caption>vol.</caption><number>19</number></detail><extent unit="pages"><start>617</start><end>23</end></extent></part><relatedItem type="host"><titleInfo><title>Oncogene</title></titleInfo><part><date>2000</date><detail type="volume"><caption>vol.</caption><number>19</number></detail><extent unit="pages"><start>617</start><end>23</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0033"><titleInfo><title>Survivin gene silencing sensitizes prostate cancer cells to selenium growth inhibition</title></titleInfo><name type="personal"><namePart type="given">X</namePart><namePart type="family">Liu</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R</namePart><namePart type="family">Gao</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Y</namePart><namePart type="family">Dong</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Liu X, Gao R, Dong Y, et al. Survivin gene silencing sensitizes prostate cancer cells to selenium growth inhibition. BMC Cancer 2010; 10: 418.</note><part><date>2010</date><detail type="volume"><caption>vol.</caption><number>10</number></detail><extent unit="pages"><start>418</start></extent></part><relatedItem type="host"><titleInfo><title>BMC Cancer</title></titleInfo><part><date>2010</date><detail type="volume"><caption>vol.</caption><number>10</number></detail><extent unit="pages"><start>418</start></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0034"><titleInfo><title>Survivin expression and its clinical significance in pancreatic cancer</title></titleInfo><name type="personal"><namePart type="given">MA</namePart><namePart type="family">Lee</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">GS</namePart><namePart type="family">Park</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">HJ</namePart><namePart type="family">Lee</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Lee MA, Park GS, Lee HJ, et al. Survivin expression and its clinical significance in pancreatic cancer. BMC Cancer 2005; 5: 127.</note><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>5</number></detail><extent unit="pages"><start>127</start></extent></part><relatedItem type="host"><titleInfo><title>BMC Cancer</title></titleInfo><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>5</number></detail><extent unit="pages"><start>127</start></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0035"><titleInfo><title>Inhibitors of apoptosis proteins (IAPs) expression and their prognostic significance in hepatocellular carcinoma</title></titleInfo><name type="personal"><namePart type="given">C</namePart><namePart type="family">Augello</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">L</namePart><namePart type="family">Caruso</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Maggioni</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Augello C, Caruso L, Maggioni M, et al. Inhibitors of apoptosis proteins (IAPs) expression and their prognostic significance in hepatocellular carcinoma. BMC Cancer 2009; 9: 125.</note><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>9</number></detail><extent unit="pages"><start>125</start></extent></part><relatedItem type="host"><titleInfo><title>BMC Cancer</title></titleInfo><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>9</number></detail><extent unit="pages"><start>125</start></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0036"><titleInfo><title>Overexpression of survivin initiates hematologic malignancies in vivo</title></titleInfo><name type="personal"><namePart type="given">S</namePart><namePart type="family">Small</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">G</namePart><namePart type="family">Keerthivasan</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Z</namePart><namePart type="family">Huang</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Small S, Keerthivasan G, Huang Z, et al. Overexpression of survivin initiates hematologic malignancies in vivo. Leukemia 2010; 24: 1920–6.</note><part><date>2010</date><detail type="volume"><caption>vol.</caption><number>24</number></detail><extent unit="pages"><start>1920</start><end>6</end></extent></part><relatedItem type="host"><titleInfo><title>Leukemia</title></titleInfo><part><date>2010</date><detail type="volume"><caption>vol.</caption><number>24</number></detail><extent unit="pages"><start>1920</start><end>6</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0037"><titleInfo><title>Survivin and leukemia</title></titleInfo><name type="personal"><namePart type="given">XL</namePart><namePart type="family">Cong</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">ZC</namePart><namePart type="family">Han</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Cong XL, Han ZC. Survivin and leukemia. Int J Hematol 2004; 80: 232–8.</note><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>80</number></detail><extent unit="pages"><start>232</start><end>8</end></extent></part><relatedItem type="host"><titleInfo><title>Int J Hematol</title></titleInfo><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>80</number></detail><extent unit="pages"><start>232</start><end>8</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0038"><titleInfo><title>Multicenter phase II trial of YM155, a small‐molecule suppressor of survivin, in patients with advanced, refractory, non‐small‐cell lung cancer</title></titleInfo><name type="personal"><namePart type="given">G</namePart><namePart type="family">Giaccone</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P</namePart><namePart type="family">Zatloukal</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Roubec</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Giaccone G, Zatloukal P, Roubec J, et al. Multicenter phase II trial of YM155, a small‐molecule suppressor of survivin, in patients with advanced, refractory, non‐small‐cell lung cancer. J Clin Oncol 2009; 27: 4481–6.</note><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>27</number></detail><extent unit="pages"><start>4481</start><end>6</end></extent></part><relatedItem type="host"><titleInfo><title>J Clin Oncol</title></titleInfo><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>27</number></detail><extent unit="pages"><start>4481</start><end>6</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0039"><titleInfo><title>Phase I study of YM155, a novel survivin suppressant, in patients with advanced solid tumors</title></titleInfo><name type="personal"><namePart type="given">T</namePart><namePart type="family">Satoh</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">I</namePart><namePart type="family">Okamoto</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Miyazaki</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Satoh T, Okamoto I, Miyazaki M, et al. Phase I study of YM155, a novel survivin suppressant, in patients with advanced solid tumors. Clin Cancer Res 2009; 15: 3872–80.</note><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>15</number></detail><extent unit="pages"><start>3872</start><end>80</end></extent></part><relatedItem type="host"><titleInfo><title>Clin Cancer Res</title></titleInfo><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>15</number></detail><extent unit="pages"><start>3872</start><end>80</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0040"><titleInfo><title>Immunohistochemical analysis of bcl‐2, bax, bcl‐X, and mcl‐1 expression in prostate cancers</title></titleInfo><name type="personal"><namePart type="given">M</namePart><namePart type="family">Krajewska</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Krajewski</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JI</namePart><namePart type="family">Epstein</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Krajewska M, Krajewski S, Epstein JI, et al. Immunohistochemical analysis of bcl‐2, bax, bcl‐X, and mcl‐1 expression in prostate cancers. Am J Pathol 1996; 148: 1567–76.</note><part><date>1996</date><detail type="volume"><caption>vol.</caption><number>148</number></detail><extent unit="pages"><start>1567</start><end>76</end></extent></part><relatedItem type="host"><titleInfo><title>Am J Pathol</title></titleInfo><part><date>1996</date><detail type="volume"><caption>vol.</caption><number>148</number></detail><extent unit="pages"><start>1567</start><end>76</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0041"><titleInfo><title>Mcl‐1 regulates survival and sensitivity to diverse apoptotic stimuli in human non‐small cell lung cancer cells</title></titleInfo><name type="personal"><namePart type="given">L</namePart><namePart type="family">Song</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">D</namePart><namePart type="family">Coppola</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Livingston</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Song L, Coppola D, Livingston S, et al. Mcl‐1 regulates survival and sensitivity to diverse apoptotic stimuli in human non‐small cell lung cancer cells. Cancer Biol Ther 2005; 4: 267–76.</note><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>4</number></detail><extent unit="pages"><start>267</start><end>76</end></extent></part><relatedItem type="host"><titleInfo><title>Cancer Biol Ther</title></titleInfo><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>4</number></detail><extent unit="pages"><start>267</start><end>76</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0042"><titleInfo><title>Mcl‐1 is an anti‐apoptotic factor for human hepatocellular carcinoma</title></titleInfo><name type="personal"><namePart type="given">B</namePart><namePart type="family">Fleischer</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H</namePart><namePart type="family">Schulze‐Bergkamen</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Schuchmann</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Fleischer B, Schulze‐Bergkamen H, Schuchmann M, et al. Mcl‐1 is an anti‐apoptotic factor for human hepatocellular carcinoma. Int J Oncol 2006; 28: 25–32.</note><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>28</number></detail><extent unit="pages"><start>25</start><end>32</end></extent></part><relatedItem type="host"><titleInfo><title>Int J Oncol</title></titleInfo><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>28</number></detail><extent unit="pages"><start>25</start><end>32</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0043"><titleInfo><title>Apoptosis induced by the kinase inhibitor BAY 43‐9006 in human leukemia cells involves down‐regulation of Mcl‐1 through inhibition of translation</title></titleInfo><name type="personal"><namePart type="given">M</namePart><namePart type="family">Rahmani</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">EM</namePart><namePart type="family">Davis</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Bauer</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Rahmani M, Davis EM, Bauer C, et al. Apoptosis induced by the kinase inhibitor BAY 43‐9006 in human leukemia cells involves down‐regulation of Mcl‐1 through inhibition of translation. J Biol Chem 2005; 280: 35217–27.</note><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>280</number></detail><extent unit="pages"><start>35217</start><end>27</end></extent></part><relatedItem type="host"><titleInfo><title>J Biol Chem</title></titleInfo><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>280</number></detail><extent unit="pages"><start>35217</start><end>27</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0044"><titleInfo><title>Elimination of Mcl‐1 is required for the initiation of apoptosis following ultraviolet irradiation</title></titleInfo><name type="personal"><namePart type="given">D</namePart><namePart type="family">Nijhawan</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Fang</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">E</namePart><namePart type="family">Traer</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Nijhawan D, Fang M, Traer E, et al. Elimination of Mcl‐1 is required for the initiation of apoptosis following ultraviolet irradiation. Genes Dev 2003; 17: 1475–86.</note><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>17</number></detail><extent unit="pages"><start>1475</start><end>86</end></extent></part><relatedItem type="host"><titleInfo><title>Genes Dev</title></titleInfo><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>17</number></detail><extent unit="pages"><start>1475</start><end>86</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0045"><titleInfo><title>Myeloid cell leukemia‐1 is a key molecular target for mithramycin A‐induced apoptosis in androgen‐independent prostate cancer cells and a tumor xenograft animal model</title></titleInfo><name type="personal"><namePart type="given">ES</namePart><namePart type="family">Choi</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JY</namePart><namePart type="family">Jung</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JS</namePart><namePart type="family">Lee</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Choi ES, Jung JY, Lee JS, et al. Myeloid cell leukemia‐1 is a key molecular target for mithramycin A‐induced apoptosis in androgen‐independent prostate cancer cells and a tumor xenograft animal model. Cancer Lett 2013; 328: 65–72.</note><part><date>2013</date><detail type="volume"><caption>vol.</caption><number>328</number></detail><extent unit="pages"><start>65</start><end>72</end></extent></part><relatedItem type="host"><titleInfo><title>Cancer Lett</title></titleInfo><part><date>2013</date><detail type="volume"><caption>vol.</caption><number>328</number></detail><extent unit="pages"><start>65</start><end>72</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0046"><titleInfo><title>YM155 induces EGFR suppression in pancreatic cancer cells</title></titleInfo><name type="personal"><namePart type="given">YS</namePart><namePart type="family">Na</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">SJ</namePart><namePart type="family">Yang</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">SM</namePart><namePart type="family">Kim</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Na YS, Yang SJ, Kim SM, et al. YM155 induces EGFR suppression in pancreatic cancer cells. PLoS ONE 2012; 7: e38625.</note><part><date>2012</date><detail type="volume"><caption>vol.</caption><number>7</number></detail><extent unit="pages"><start>e38625</start></extent></part><relatedItem type="host"><titleInfo><title>PLoS ONE</title></titleInfo><part><date>2012</date><detail type="volume"><caption>vol.</caption><number>7</number></detail><extent unit="pages"><start>e38625</start></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0047"><titleInfo><title>Increased expression of AP2 and Sp1 transcription factors in human thyroid tumors: a role in NIS expression regulation?</title></titleInfo><name type="personal"><namePart type="given">E</namePart><namePart type="family">Chiefari</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Brunetti</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">F</namePart><namePart type="family">Arturi</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Chiefari E, Brunetti A, Arturi F, et al. Increased expression of AP2 and Sp1 transcription factors in human thyroid tumors: a role in NIS expression regulation? BMC Cancer 2002; 2: 35.</note><part><date>2002</date><detail type="volume"><caption>vol.</caption><number>2</number></detail><extent unit="pages"><start>35</start></extent></part><relatedItem type="host"><titleInfo><title>BMC Cancer</title></titleInfo><part><date>2002</date><detail type="volume"><caption>vol.</caption><number>2</number></detail><extent unit="pages"><start>35</start></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="jop12299-cit-0048"><titleInfo><title>Association between expression of transcription factor Sp1 and increased vascular endothelial growth factor expression, advanced stage, and poor survival in patients with resected gastric cancer</title></titleInfo><name type="personal"><namePart type="given">JC</namePart><namePart type="family">Yao</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">L</namePart><namePart type="family">Wang</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">D</namePart><namePart type="family">Wei</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Yao JC, Wang L, Wei D, et al. Association between expression of transcription factor Sp1 and increased vascular endothelial growth factor expression, advanced stage, and poor survival in patients with resected gastric cancer. Clin Cancer Res 2004; 10: 4109–17.</note><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>10</number></detail><extent unit="pages"><start>4109</start><end>17</end></extent></part><relatedItem type="host"><titleInfo><title>Clin Cancer Res</title></titleInfo><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>10</number></detail><extent unit="pages"><start>4109</start><end>17</end></extent></part></relatedItem></relatedItem><identifier type="istex">8F4DF8D109CAD6AFD3938F4E915759780F79AD2A</identifier><identifier type="ark">ark:/67375/WNG-K8XGFKSM-V</identifier><identifier type="DOI">10.1111/jop.12299</identifier><identifier type="ArticleID">JOP12299</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd© 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-L0C46X92-X">wiley</recordContentSource><recordOrigin>Converted from (version ) to MODS version 3.6.</recordOrigin><recordCreationDate encoding="w3cdtf">2019-11-15</recordCreationDate></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-K8XGFKSM-V/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Sante/explor/ChloroquineV1/Data/Istex/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 001459 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Istex/Corpus/biblio.hfd -nk 001459 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Sante
|area= ChloroquineV1
|flux= Istex
|étape= Corpus
|type= RBID
|clé= ISTEX:8F4DF8D109CAD6AFD3938F4E915759780F79AD2A
|texte= YM155 induces apoptosis through downregulation of specificity protein 1 and myeloid cell leukemia‐1 in human oral cancer cell lines
}}
| This area was generated with Dilib version V0.6.33. |  |