Synthesized Pheophorbide a‐mediated photodynamic therapy induced apoptosis and autophagy in human oral squamous carcinoma cells
Identifieur interne : 002380 ( Istex/Corpus ); précédent : 002379; suivant : 002381Synthesized Pheophorbide a‐mediated photodynamic therapy induced apoptosis and autophagy in human oral squamous carcinoma cells
Auteurs : Mee Young Ahn ; Hyo-Eun Yoon ; Seong-Min Kwon ; Jun Lee ; Seung-Ki Min ; Yong-Chul Kim ; Sang-Gun Ahn ; Jung-Hoon YoonSource :
- Journal of Oral Pathology & Medicine [ 0904-2512 ] ; 2013-01.
English descriptors
- Teeft :
- Acridine, Actin, Actin levels, Annexin, Annexin apoptotic cells, Apoptosis, Apoptotic, Apoptotic cell death, Apoptotic cells, Assay, Autophagy, Autophagy inhibition, Autophagy inhibitor, Beckman coulter, Carcinoma, Cell death, Cell proliferation, Cell survival, Cell viability, Control cells, Culture medium, Cytometry analysis, Daejeon, Exclusion assay, Hmgb1, Human oscc cells, Independent experiments, Laser, Mitochondrial membrane, Molecular mechanisms, Molecular probes, Neck cancer, Necrosis, Necrotic, Necrotic cell death, Necrotic cells, Oral pathol, Oscc, Oscc cells, Parp, Parp cleavage, Pathol, Pathway, Photodynamic, Photodynamic therapy, Protein levels, Reactive oxygen species, Representative bands, Untreated control, Uorescence, Uorescence microscope, Uorescence microscopy, Viable cells, Western blot analysis, Wonkwang university.
Abstract
Background: Pheophorbide a (Pa) is a chlorine‐based photosensitizer derived from an ethnopharmacological herb, and our group recently synthesized Pa by the removal of a magnesium ion and a phytyl group from chlorophyll‐a. In this study, the effect of photodynamic therapy (PDT) with synthesized Pa was examined in a human oral squamous cell carcinoma (OSCC) cells. Methods: Cells were treated with PDT with Pa, and reactive oxygen species (ROS) and mitochondrial membrane potential [ΔΨ (m)] were examined. Apoptosis was measured using annexin V staining and immunoblot. Autophagy was characterized by the increase in LC3B‐II and the formation of autophagosome and acidic vesicular organelles (AVOs). Results: Pa‐PDT inhibited the proliferation of OSCC cells in a dose‐dependent manner. Pa‐PDT increased the number of apoptotic cells by inactivating ERK pathway. Pa‐PDT also induced autophagy in OSCC cells evidenced by the increased levels of LC3 type II expression and the accumulation of AVOs. The inhibition of autophagy enhanced Pa‐PDT‐mediated cytotoxicity through an increase in necrosis. Conclusions: These results suggest that synthesized Pa‐PDT exerts anti‐tumor effects by inducing apoptosis and autophagy and provide novel evidence that Pa‐PDT induces autophagy, and autophagy inhibition enhances Pa‐PDT‐mediated necrosis in OSCC cells.
Url:
DOI: 10.1111/j.1600-0714.2012.01187.x
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ISTEX:297AFD5ED2803EC0AAF5A9BC760DB8D5516396A6Le document en format XML
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Hyo Un" uniqKey="Yoon H" first="Hyo-Eun" last="Yoon">Hyo-Eun Yoon</name><affiliation><mods:affiliation>Department of Pathology, Research Center for Oral disease Regulation of the Aged, School of Dentistry, Chosun University, Gwangju, Korea</mods:affiliation></affiliation></author><author><name sortKey="Kwon, Seong In" sort="Kwon, Seong In" uniqKey="Kwon S" first="Seong-Min" last="Kwon">Seong-Min Kwon</name><affiliation><mods:affiliation>Department of Pathology, Research Center for Oral disease Regulation of the Aged, School of Dentistry, Chosun University, Gwangju, Korea</mods:affiliation></affiliation></author><author><name sortKey="Lee, Jun" sort="Lee, Jun" uniqKey="Lee J" first="Jun" last="Lee">Jun Lee</name><affiliation><mods:affiliation>Department of Oral & Maxillofacial Surgery, College of Dentistry, Daejeon Dental Hospital, Wonkwang Bone Regeneration Institute, Wonkwang University, Daejeon, Korea</mods:affiliation></affiliation></author><author><name sortKey="Min, Seung I" sort="Min, Seung I" uniqKey="Min S" first="Seung-Ki" last="Min">Seung-Ki Min</name><affiliation><mods:affiliation>Department of Oral & Maxillofacial Surgery, College of Dentistry, Daejeon Dental Hospital, Wonkwang Bone Regeneration Institute, Wonkwang University, Daejeon, Korea</mods:affiliation></affiliation></author><author><name sortKey="Kim, Yong Hul" sort="Kim, Yong Hul" uniqKey="Kim Y" first="Yong-Chul" last="Kim">Yong-Chul Kim</name><affiliation><mods:affiliation>Department of Life Science, Gwangju Institute of Science and Technology, Gwangju, Korea</mods:affiliation></affiliation></author><author><name sortKey="Ahn, Sang Un" sort="Ahn, Sang Un" uniqKey="Ahn S" first="Sang-Gun" last="Ahn">Sang-Gun Ahn</name><affiliation><mods:affiliation>Department of Pathology, Research Center for Oral disease Regulation of the Aged, School of Dentistry, Chosun University, Gwangju, Korea</mods:affiliation></affiliation></author><author><name sortKey="Yoon, Jung Oon" sort="Yoon, Jung Oon" uniqKey="Yoon J" first="Jung-Hoon" last="Yoon">Jung-Hoon Yoon</name><affiliation><mods:affiliation>Department of Oral & Maxillofacial Pathology, College of Dentistry, Daejeon Dental Hospital, Wonkwang Bone Regeneration Institute, Wonkwang University, Daejeon, Korea</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 ORAL PATHOLOGY MEDICINE</title><idno type="ISSN">0904-2512</idno><idno type="eISSN">1600-0714</idno><imprint><biblScope unit="vol">42</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="17">17</biblScope><biblScope unit="page" to="25">25</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2013-01">2013-01</date></imprint><idno type="ISSN">0904-2512</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0904-2512</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Acridine</term><term>Actin</term><term>Actin levels</term><term>Annexin</term><term>Annexin apoptotic cells</term><term>Apoptosis</term><term>Apoptotic</term><term>Apoptotic cell death</term><term>Apoptotic cells</term><term>Assay</term><term>Autophagy</term><term>Autophagy inhibition</term><term>Autophagy inhibitor</term><term>Beckman coulter</term><term>Carcinoma</term><term>Cell death</term><term>Cell proliferation</term><term>Cell survival</term><term>Cell viability</term><term>Control cells</term><term>Culture medium</term><term>Cytometry analysis</term><term>Daejeon</term><term>Exclusion assay</term><term>Hmgb1</term><term>Human oscc cells</term><term>Independent experiments</term><term>Laser</term><term>Mitochondrial membrane</term><term>Molecular mechanisms</term><term>Molecular probes</term><term>Neck cancer</term><term>Necrosis</term><term>Necrotic</term><term>Necrotic cell death</term><term>Necrotic cells</term><term>Oral pathol</term><term>Oscc</term><term>Oscc cells</term><term>Parp</term><term>Parp cleavage</term><term>Pathol</term><term>Pathway</term><term>Photodynamic</term><term>Photodynamic therapy</term><term>Protein levels</term><term>Reactive oxygen species</term><term>Representative bands</term><term>Untreated control</term><term>Uorescence</term><term>Uorescence microscope</term><term>Uorescence microscopy</term><term>Viable cells</term><term>Western blot analysis</term><term>Wonkwang university</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Background: Pheophorbide a (Pa) is a chlorine‐based photosensitizer derived from an ethnopharmacological herb, and our group recently synthesized Pa by the removal of a magnesium ion and a phytyl group from chlorophyll‐a. In this study, the effect of photodynamic therapy (PDT) with synthesized Pa was examined in a human oral squamous cell carcinoma (OSCC) cells. Methods: Cells were treated with PDT with Pa, and reactive oxygen species (ROS) and mitochondrial membrane potential [ΔΨ (m)] were examined. Apoptosis was measured using annexin V staining and immunoblot. Autophagy was characterized by the increase in LC3B‐II and the formation of autophagosome and acidic vesicular organelles (AVOs). Results: Pa‐PDT inhibited the proliferation of OSCC cells in a dose‐dependent manner. Pa‐PDT increased the number of apoptotic cells by inactivating ERK pathway. Pa‐PDT also induced autophagy in OSCC cells evidenced by the increased levels of LC3 type II expression and the accumulation of AVOs. The inhibition of autophagy enhanced Pa‐PDT‐mediated cytotoxicity through an increase in necrosis. Conclusions: These results suggest that synthesized Pa‐PDT exerts anti‐tumor effects by inducing apoptosis and autophagy and provide novel evidence that Pa‐PDT induces autophagy, and autophagy inhibition enhances Pa‐PDT‐mediated necrosis in OSCC cells.</div></front></TEI><istex><corpusName>wiley</corpusName><keywords><teeft><json:string>autophagy</json:string><json:string>apoptosis</json:string><json:string>oscc</json:string><json:string>photodynamic</json:string><json:string>uorescence</json:string><json:string>laser</json:string><json:string>photodynamic therapy</json:string><json:string>apoptotic</json:string><json:string>cell death</json:string><json:string>annexin</json:string><json:string>pathol</json:string><json:string>oral pathol</json:string><json:string>uorescence microscopy</json:string><json:string>parp</json:string><json:string>actin</json:string><json:string>pathway</json:string><json:string>independent experiments</json:string><json:string>oscc cells</json:string><json:string>assay</json:string><json:string>hmgb1</json:string><json:string>acridine</json:string><json:string>cell viability</json:string><json:string>daejeon</json:string><json:string>apoptotic cell death</json:string><json:string>necrotic cell death</json:string><json:string>autophagy inhibitor</json:string><json:string>mitochondrial membrane</json:string><json:string>western blot analysis</json:string><json:string>autophagy inhibition</json:string><json:string>necrotic</json:string><json:string>exclusion assay</json:string><json:string>uorescence microscope</json:string><json:string>cell proliferation</json:string><json:string>molecular mechanisms</json:string><json:string>carcinoma</json:string><json:string>control cells</json:string><json:string>molecular probes</json:string><json:string>beckman coulter</json:string><json:string>annexin apoptotic cells</json:string><json:string>neck cancer</json:string><json:string>human oscc cells</json:string><json:string>necrotic cells</json:string><json:string>viable cells</json:string><json:string>reactive oxygen species</json:string><json:string>apoptotic cells</json:string><json:string>wonkwang university</json:string><json:string>untreated control</json:string><json:string>parp cleavage</json:string><json:string>cytometry analysis</json:string><json:string>culture medium</json:string><json:string>protein levels</json:string><json:string>actin levels</json:string><json:string>representative bands</json:string><json:string>cell survival</json:string><json:string>necrosis</json:string></teeft></keywords><author><json:item><name>Mee Young Ahn</name><affiliations><json:string>Department of Pathology, Research Center for Oral disease Regulation of the Aged, School of Dentistry, Chosun University, Gwangju, Korea</json:string></affiliations></json:item><json:item><name>Hyo‐Eun Yoon</name><affiliations><json:string>Department of Pathology, Research Center for Oral disease Regulation of the Aged, School of Dentistry, Chosun University, Gwangju, Korea</json:string></affiliations></json:item><json:item><name>Seong‐Min Kwon</name><affiliations><json:string>Department of Pathology, Research Center for Oral disease Regulation of the Aged, School of Dentistry, Chosun University, Gwangju, Korea</json:string></affiliations></json:item><json:item><name>Jun Lee</name><affiliations><json:string>Department of Oral & Maxillofacial Surgery, College of Dentistry, Daejeon Dental Hospital, Wonkwang Bone Regeneration Institute, Wonkwang University, Daejeon, Korea</json:string></affiliations></json:item><json:item><name>Seung‐Ki Min</name><affiliations><json:string>Department of Oral & Maxillofacial Surgery, College of Dentistry, Daejeon Dental Hospital, Wonkwang Bone Regeneration Institute, Wonkwang University, Daejeon, Korea</json:string></affiliations></json:item><json:item><name>Yong‐Chul Kim</name><affiliations><json:string>Department of Life Science, Gwangju Institute of Science and Technology, Gwangju, Korea</json:string></affiliations></json:item><json:item><name>Sang‐Gun Ahn</name><affiliations><json:string>Department of Pathology, Research Center for Oral disease Regulation of the Aged, School of Dentistry, Chosun University, Gwangju, Korea</json:string></affiliations></json:item><json:item><name>Jung‐Hoon Yoon</name><affiliations><json:string>Department of Oral & Maxillofacial Pathology, College of Dentistry, Daejeon Dental Hospital, Wonkwang Bone Regeneration Institute, Wonkwang University, Daejeon, Korea</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>autophagy</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>necrosis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>oral sqaumous cell carcinoma</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>synthesized Pa‐PDT</value></json:item></subject><articleId><json:string>JOP1187</json:string></articleId><arkIstex>ark:/67375/WNG-6M2T2Q82-L</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Background: Pheophorbide a (Pa) is a chlorine‐based photosensitizer derived from an ethnopharmacological herb, and our group recently synthesized Pa by the removal of a magnesium ion and a phytyl group from chlorophyll‐a. In this study, the effect of photodynamic therapy (PDT) with synthesized Pa was examined in a human oral squamous cell carcinoma (OSCC) cells. Methods: Cells were treated with PDT with Pa, and reactive oxygen species (ROS) and mitochondrial membrane potential [ΔΨ (m)] were examined. Apoptosis was measured using annexin V staining and immunoblot. Autophagy was characterized by the increase in LC3B‐II and the formation of autophagosome and acidic vesicular organelles (AVOs). Results: Pa‐PDT inhibited the proliferation of OSCC cells in a dose‐dependent manner. Pa‐PDT increased the number of apoptotic cells by inactivating ERK pathway. Pa‐PDT also induced autophagy in OSCC cells evidenced by the increased levels of LC3 type II expression and the accumulation of AVOs. The inhibition of autophagy enhanced Pa‐PDT‐mediated cytotoxicity through an increase in necrosis. Conclusions: These results suggest that synthesized Pa‐PDT exerts anti‐tumor effects by inducing apoptosis and autophagy and provide novel evidence that Pa‐PDT induces autophagy, and autophagy inhibition enhances Pa‐PDT‐mediated necrosis in OSCC cells.</abstract><qualityIndicators><score>9.061</score><pdfWordCount>4757</pdfWordCount><pdfCharCount>30455</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>9</pdfPageCount><pdfPageSize>595.276 x 782.362 pts</pdfPageSize><pdfWordsPerPage>529</pdfWordsPerPage><pdfText>true</pdfText><refBibsNative>true</refBibsNative><abstractWordCount>192</abstractWordCount><abstractCharCount>1351</abstractCharCount><keywordCount>5</keywordCount></qualityIndicators><title>Synthesized Pheophorbide a‐mediated photodynamic therapy induced apoptosis and autophagy in human oral squamous carcinoma cells</title><pmid><json:string>22742535</json:string></pmid><genre><json:string>article</json:string></genre><host><title>Journal of Oral Pathology & 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type="short">Anti‐tumor effect of Pa‐PDT in OSCC</title><author xml:id="author-0000"><persName><forename type="first">Mee Young</forename><surname>Ahn</surname></persName><affiliation><orgName type="department">Department of Pathology</orgName><orgName type="institution">Research Center for Oral disease Regulation of the Aged</orgName><orgName type="department">School of Dentistry</orgName><orgName type="institution">Chosun University</orgName><address><addrLine>Gwangju</addrLine><addrLine>Korea</addrLine></address></affiliation></author><author xml:id="author-0001"><persName><forename type="first">Hyo‐Eun</forename><surname>Yoon</surname></persName><affiliation><orgName type="department">Department of Pathology</orgName><orgName type="institution">Research Center for Oral disease Regulation of the Aged</orgName><orgName type="department">School of Dentistry</orgName><orgName type="institution">Chosun University</orgName><address><addrLine>Gwangju</addrLine><addrLine>Korea</addrLine></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">Seong‐Min</forename><surname>Kwon</surname></persName><affiliation><orgName type="department">Department of Pathology</orgName><orgName type="institution">Research Center for Oral disease Regulation of the Aged</orgName><orgName type="department">School of Dentistry</orgName><orgName type="institution">Chosun University</orgName><address><addrLine>Gwangju</addrLine><addrLine>Korea</addrLine></address></affiliation></author><author xml:id="author-0003"><persName><forename type="first">Jun</forename><surname>Lee</surname></persName><affiliation><orgName type="division">Department of Oral & Maxillofacial Surgery</orgName><orgName type="institution">College of Dentistry</orgName><orgName type="institution">Daejeon Dental Hospital</orgName><orgName type="institution">Wonkwang Bone Regeneration Institute</orgName><orgName type="institution">Wonkwang University</orgName><address><addrLine>Daejeon</addrLine><addrLine>Korea</addrLine></address></affiliation></author><author xml:id="author-0004"><persName><forename type="first">Seung‐Ki</forename><surname>Min</surname></persName><affiliation><orgName type="division">Department of Oral & Maxillofacial Surgery</orgName><orgName type="institution">College of Dentistry</orgName><orgName type="institution">Daejeon Dental Hospital</orgName><orgName type="institution">Wonkwang Bone Regeneration Institute</orgName><orgName type="institution">Wonkwang University</orgName><address><addrLine>Daejeon</addrLine><addrLine>Korea</addrLine></address></affiliation></author><author xml:id="author-0005"><persName><forename type="first">Yong‐Chul</forename><surname>Kim</surname></persName><affiliation><orgName type="division">Department of Life Science</orgName><orgName type="institution">Gwangju Institute of Science and Technology</orgName><address><addrLine>Gwangju</addrLine><addrLine>Korea</addrLine></address></affiliation></author><author xml:id="author-0006"><persName><forename type="first">Sang‐Gun</forename><surname>Ahn</surname></persName><affiliation><orgName type="department">Department of Pathology</orgName><orgName type="institution">Research Center for Oral disease Regulation of the Aged</orgName><orgName type="department">School of Dentistry</orgName><orgName type="institution">Chosun University</orgName><address><addrLine>Gwangju</addrLine><addrLine>Korea</addrLine></address></affiliation></author><author xml:id="author-0007"><persName><forename type="first">Jung‐Hoon</forename><surname>Yoon</surname></persName><affiliation><orgName type="department">Department of Oral & Maxillofacial Pathology</orgName><orgName type="institution">College of Dentistry</orgName><orgName type="institution">Daejeon Dental Hospital</orgName><orgName type="institution">Wonkwang Bone Regeneration Institute</orgName><orgName type="institution">Wonkwang University</orgName><address><addrLine>Daejeon</addrLine><addrLine>Korea</addrLine></address></affiliation></author><idno type="istex">297AFD5ED2803EC0AAF5A9BC760DB8D5516396A6</idno><idno type="ark">ark:/67375/WNG-6M2T2Q82-L</idno><idno type="DOI">10.1111/j.1600-0714.2012.01187.x</idno><idno type="unit">JOP1187</idno><idno type="toTypesetVersion">file:JOP.JOP1187.pdf</idno></analytic><monogr><title level="j" type="main">Journal of Oral Pathology & Medicine</title><title level="j" type="alt">JOURNAL ORAL PATHOLOGY 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.2012.42.issue-1</idno><idno type="product">JOP</idno><idno type="publisherDivision">ST</idno><imprint><biblScope unit="vol">42</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="17">17</biblScope><biblScope unit="page" to="25">25</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2013-01"></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 xml:lang="en" style="main"><p><hi rend="bold">Background: </hi> Pheophorbide a (Pa) is a chlorine‐based photosensitizer derived from an ethnopharmacological herb, and our group recently synthesized Pa by the removal of a magnesium ion and a phytyl group from chlorophyll‐a. In this study, the effect of photodynamic therapy (PDT) with synthesized Pa was examined in a human oral squamous cell carcinoma (OSCC) cells.</p><p><hi rend="bold">Methods: </hi> Cells were treated with PDT with Pa, and reactive oxygen species (ROS) and mitochondrial membrane potential [ΔΨ (m)] were examined. Apoptosis was measured using annexin V staining and immunoblot. Autophagy was characterized by the increase in LC3B‐II and the formation of autophagosome and acidic vesicular organelles (AVOs).</p><p><hi rend="bold">Results: </hi> Pa‐PDT inhibited the proliferation of OSCC cells in a dose‐dependent manner. Pa‐PDT increased the number of apoptotic cells by inactivating ERK pathway. Pa‐PDT also induced autophagy in OSCC cells evidenced by the increased levels of LC3 type II expression and the accumulation of AVOs. The inhibition of autophagy enhanced Pa‐PDT‐mediated cytotoxicity through an increase in necrosis.</p><p><hi rend="bold">Conclusions: </hi> These results suggest that synthesized Pa‐PDT exerts anti‐tumor effects by inducing apoptosis and autophagy and provide novel evidence that Pa‐PDT induces autophagy, and autophagy inhibition enhances Pa‐PDT‐mediated necrosis in OSCC cells.</p></abstract><textClass><keywords xml:lang="en"><term xml:id="k1">apoptosis</term><term xml:id="k2">autophagy</term><term xml:id="k3">necrosis</term><term xml:id="k4">oral sqaumous cell carcinoma</term><term xml:id="k5">synthesized Pa‐PDT</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-6M2T2Q82-L/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 version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><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><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="JOURNAL ORAL PATHOLOGY MEDICINE">Journal of Oral Pathology & Medicine</title></titleGroup></publicationMeta><publicationMeta level="part" position="01101"><doi origin="wiley">10.1111/jop.2012.42.issue-1</doi><numberingGroup><numbering type="journalVolume" number="42">42</numbering><numbering type="journalIssue" number="1">1</numbering></numberingGroup><coverDate startDate="2013-01">January 2013</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="3" status="forIssue"><doi origin="wiley">10.1111/j.1600-0714.2012.01187.x</doi><idGroup><id type="unit" value="JOP1187"></id></idGroup><titleGroup><title type="tocHeading1"><i>Original articles</i></title></titleGroup><copyright>© 2012 John Wiley & Sons A/S</copyright><eventGroup><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:3.1.9 mode:FullText" date="2012-12-19"></event><event agent="SPS" date="2012-12-20" type="xmlCorrected"></event><event type="publishedOnlineEarlyUnpaginated" date="2012-06-28"></event><event type="publishedOnlineFinalForm" date="2013-01-03"></event><event type="firstOnline" date="2012-06-28"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-31"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.6.4 mode:FullText" date="2015-10-01"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="17">17</numbering><numbering type="pageLast" number="25">25</numbering></numberingGroup><correspondenceTo>Sang‐Gun Ahn, PhD, Department of Pathology, School of Dentistry, Chosun University 375 Dong‐Gu, Seoseok‐dong, Gwangju, 501‐759 Korea. Tel: +82 62 230 6879, Fax: +82 62 223 3205 and Jung‐Hoon Yoon, DDS, PhD, Department of Oral & Maxillofacial Pathology, College of Dentistry, Daejeon Dental Hospital, Wonkwang University, Daejeon 302‐120, Korea. Tel: +82 42 366 1146, Fax: +82 42 366 1115, E‐mails: <email>ahnsg@chosun.ac.kr</email>; <email>opathyoon@wku.ac.kr</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:JOP.JOP1187.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Accepted for publication May 24, 2012</unparsedEditorialHistory><countGroup><count type="figureTotal" number="6"></count><count type="tableTotal" number="0"></count></countGroup><titleGroup><title type="main">Synthesized Pheophorbide a‐mediated photodynamic therapy induced apoptosis and autophagy in human oral squamous carcinoma cells</title><title type="shortAuthors">Ahn et al.</title><title type="short"><b>Anti‐tumor effect of Pa‐PDT in OSCC</b></title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>Mee Young</givenNames><familyName>Ahn</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>Hyo‐Eun</givenNames><familyName>Yoon</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1"><personName><givenNames>Seong‐Min</givenNames><familyName>Kwon</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a2"><personName><givenNames>Jun</givenNames><familyName>Lee</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a2"><personName><givenNames>Seung‐Ki</givenNames><familyName>Min</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a3"><personName><givenNames>Yong‐Chul</givenNames><familyName>Kim</familyName></personName></creator><creator creatorRole="author" xml:id="cr7" affiliationRef="#a1"><personName><givenNames>Sang‐Gun</givenNames><familyName>Ahn</familyName></personName></creator><creator creatorRole="author" xml:id="cr8" affiliationRef="#a4"><personName><givenNames>Jung‐Hoon</givenNames><familyName>Yoon</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1"><unparsedAffiliation>Department of Pathology, Research Center for Oral disease Regulation of the Aged, School of Dentistry, Chosun University, Gwangju, Korea</unparsedAffiliation></affiliation><affiliation xml:id="a2"><unparsedAffiliation>Department of Oral & Maxillofacial Surgery, College of Dentistry, Daejeon Dental Hospital, Wonkwang Bone Regeneration Institute, Wonkwang University, Daejeon, Korea</unparsedAffiliation></affiliation><affiliation xml:id="a3"><unparsedAffiliation>Department of Life Science, Gwangju Institute of Science and Technology, Gwangju, Korea</unparsedAffiliation></affiliation><affiliation xml:id="a4"><unparsedAffiliation>Department of Oral & Maxillofacial Pathology, College of Dentistry, Daejeon Dental Hospital, Wonkwang Bone Regeneration Institute, Wonkwang University, Daejeon, Korea</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">apoptosis</keyword><keyword xml:id="k2">autophagy</keyword><keyword xml:id="k3">necrosis</keyword><keyword xml:id="k4">oral sqaumous cell carcinoma</keyword><keyword xml:id="k5">synthesized Pa‐PDT</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p><b>Background: </b> Pheophorbide a (Pa) is a chlorine‐based photosensitizer derived from an ethnopharmacological herb, and our group recently synthesized Pa by the removal of a magnesium ion and a phytyl group from chlorophyll‐a. In this study, the effect of photodynamic therapy (PDT) with synthesized Pa was examined in a human oral squamous cell carcinoma (OSCC) cells.</p><p><b>Methods: </b> Cells were treated with PDT with Pa, and reactive oxygen species (ROS) and mitochondrial membrane potential [ΔΨ (m)] were examined. Apoptosis was measured using annexin V staining and immunoblot. Autophagy was characterized by the increase in LC3B‐II and the formation of autophagosome and acidic vesicular organelles (AVOs).</p><p><b>Results: </b> Pa‐PDT inhibited the proliferation of OSCC cells in a dose‐dependent manner. Pa‐PDT increased the number of apoptotic cells by inactivating ERK pathway. Pa‐PDT also induced autophagy in OSCC cells evidenced by the increased levels of LC3 type II expression and the accumulation of AVOs. The inhibition of autophagy enhanced Pa‐PDT‐mediated cytotoxicity through an increase in necrosis.</p><p><b>Conclusions: </b> These results suggest that synthesized Pa‐PDT exerts anti‐tumor effects by inducing apoptosis and autophagy and provide novel evidence that Pa‐PDT induces autophagy, and autophagy inhibition enhances Pa‐PDT‐mediated necrosis in OSCC cells.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Synthesized Pheophorbide a‐mediated photodynamic therapy induced apoptosis and autophagy in human oral squamous carcinoma cells</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Anti‐tumor effect of Pa‐PDT in OSCC</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Synthesized Pheophorbide a‐mediated photodynamic therapy induced apoptosis and autophagy in human oral squamous carcinoma cells</title></titleInfo><name type="personal"><namePart type="given">Mee Young</namePart><namePart type="family">Ahn</namePart><affiliation>Department of Pathology, Research Center for Oral disease Regulation of the Aged, School of Dentistry, Chosun University, Gwangju, Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hyo‐Eun</namePart><namePart type="family">Yoon</namePart><affiliation>Department of Pathology, Research Center for Oral disease Regulation of the Aged, School of Dentistry, Chosun University, Gwangju, Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Seong‐Min</namePart><namePart type="family">Kwon</namePart><affiliation>Department of Pathology, Research Center for Oral disease Regulation of the Aged, School of Dentistry, Chosun University, Gwangju, Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jun</namePart><namePart type="family">Lee</namePart><affiliation>Department of Oral & Maxillofacial Surgery, College of Dentistry, Daejeon Dental Hospital, Wonkwang Bone Regeneration Institute, Wonkwang University, Daejeon, Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Seung‐Ki</namePart><namePart type="family">Min</namePart><affiliation>Department of Oral & Maxillofacial Surgery, College of Dentistry, Daejeon Dental Hospital, Wonkwang Bone Regeneration Institute, Wonkwang University, Daejeon, Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yong‐Chul</namePart><namePart type="family">Kim</namePart><affiliation>Department of Life Science, Gwangju Institute of Science and Technology, Gwangju, Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Sang‐Gun</namePart><namePart type="family">Ahn</namePart><affiliation>Department of Pathology, Research Center for Oral disease Regulation of the Aged, School of Dentistry, Chosun University, Gwangju, Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jung‐Hoon</namePart><namePart type="family">Yoon</namePart><affiliation>Department of Oral & Maxillofacial Pathology, College of Dentistry, Daejeon Dental Hospital, Wonkwang Bone Regeneration Institute, Wonkwang University, Daejeon, Korea</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><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2013-01</dateIssued><edition>Accepted for publication May 24, 2012</edition><copyrightDate encoding="w3cdtf">2013</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="figures">6</extent><extent unit="tables">0</extent></physicalDescription><abstract lang="en">Background: Pheophorbide a (Pa) is a chlorine‐based photosensitizer derived from an ethnopharmacological herb, and our group recently synthesized Pa by the removal of a magnesium ion and a phytyl group from chlorophyll‐a. In this study, the effect of photodynamic therapy (PDT) with synthesized Pa was examined in a human oral squamous cell carcinoma (OSCC) cells. Methods: Cells were treated with PDT with Pa, and reactive oxygen species (ROS) and mitochondrial membrane potential [ΔΨ (m)] were examined. Apoptosis was measured using annexin V staining and immunoblot. Autophagy was characterized by the increase in LC3B‐II and the formation of autophagosome and acidic vesicular organelles (AVOs). Results: Pa‐PDT inhibited the proliferation of OSCC cells in a dose‐dependent manner. Pa‐PDT increased the number of apoptotic cells by inactivating ERK pathway. Pa‐PDT also induced autophagy in OSCC cells evidenced by the increased levels of LC3 type II expression and the accumulation of AVOs. The inhibition of autophagy enhanced Pa‐PDT‐mediated cytotoxicity through an increase in necrosis. Conclusions: These results suggest that synthesized Pa‐PDT exerts anti‐tumor effects by inducing apoptosis and autophagy and provide novel evidence that Pa‐PDT induces autophagy, and autophagy inhibition enhances Pa‐PDT‐mediated necrosis in OSCC cells.</abstract><subject lang="en"><genre>keywords</genre><topic>apoptosis</topic><topic>autophagy</topic><topic>necrosis</topic><topic>oral sqaumous cell carcinoma</topic><topic>synthesized Pa‐PDT</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Oral Pathology & Medicine</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><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>2013</date><detail type="volume"><caption>vol.</caption><number>42</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>17</start><end>25</end></extent></part></relatedItem><relatedItem type="references" displayLabel="cit1"><titleInfo><title>Head and neck cancer: past, present and future</title></titleInfo><name type="personal"><namePart type="given">D</namePart><namePart type="family">Chin</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">GM</namePart><namePart type="family">Boyle</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Porceddu</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">DR</namePart><namePart type="family">Theile</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">PG</namePart><namePart type="family">Parsons</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">WB</namePart><namePart type="family">Coman</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Chin D, Boyle GM, Porceddu S, Theile DR, Parsons PG, Coman WB. 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