ChloroquineV1, PubMed, Checkpoint, bibRecord, 000376

Augmentation of NVP-BEZ235's anticancer activity against human lung cancer cells by blockage of autophagy.

Identifieur interne : 000376 ( PubMed/Checkpoint ); précédent : 000375; suivant : 000377

Augmentation of NVP-BEZ235's anticancer activity against human lung cancer cells by blockage of autophagy.

Auteurs : Cheng-Xiong Xu [États-Unis] ; Liqun Zhao ; Ping Yue ; Guofu Fang ; Hui Tao ; Taofeek K. Owonikoko ; Suresh S. Ramalingam ; Fadlo R. Khuri ; Shi-Yong Sun

Source :

Cancer biology & therapy [ 1555-8576 ] ; 2011.

RBID : pubmed:21738008

Descripteurs français

KwdFr :
- Animaux, Apoptose (), Autophagie (), Carcinome pulmonaire non à petites cellules (anatomopathologie), Carcinome pulmonaire non à petites cellules (traitement médicamenteux), Charge tumorale (), Chloroquine (pharmacologie), Chloroquine (usage thérapeutique), Femelle, Humains, Imidazoles (pharmacologie), Imidazoles (usage thérapeutique), Lignée cellulaire tumorale, Prolifération cellulaire (), Protéines proto-oncogènes c-akt (antagonistes et inhibiteurs), Protéines proto-oncogènes c-akt (métabolisme), Quinoléines (pharmacologie), Quinoléines (usage thérapeutique), Souris, Souris nude, Synergie des médicaments, Sérine-thréonine kinases TOR (antagonistes et inhibiteurs), Sérine-thréonine kinases TOR (métabolisme), Tests d'activité antitumorale sur modèle de xénogreffe, Transduction du signal, Tumeurs du poumon (anatomopathologie), Tumeurs du poumon (traitement médicamenteux).
MESH :
- anatomopathologie : Carcinome pulmonaire non à petites cellules, Tumeurs du poumon.
- antagonistes et inhibiteurs : Protéines proto-oncogènes c-akt, Sérine-thréonine kinases TOR.
- métabolisme : Protéines proto-oncogènes c-akt, Sérine-thréonine kinases TOR.
- pharmacologie : Chloroquine, Imidazoles, Quinoléines.
- traitement médicamenteux : Carcinome pulmonaire non à petites cellules, Tumeurs du poumon.
- usage thérapeutique : Chloroquine, Imidazoles, Quinoléines.
- Animaux, Apoptose, Autophagie, Charge tumorale, Femelle, Humains, Lignée cellulaire tumorale, Prolifération cellulaire, Souris, Souris nude, Synergie des médicaments, Tests d'activité antitumorale sur modèle de xénogreffe, Transduction du signal.

English descriptors

KwdEn :
- Animals, Apoptosis (drug effects), Autophagy (drug effects), Carcinoma, Non-Small-Cell Lung (drug therapy), Carcinoma, Non-Small-Cell Lung (pathology), Cell Line, Tumor, Cell Proliferation (drug effects), Chloroquine (pharmacology), Chloroquine (therapeutic use), Drug Synergism, Female, Humans, Imidazoles (pharmacology), Imidazoles (therapeutic use), Lung Neoplasms (drug therapy), Lung Neoplasms (pathology), Mice, Mice, Nude, Proto-Oncogene Proteins c-akt (antagonists & inhibitors), Proto-Oncogene Proteins c-akt (metabolism), Quinolines (pharmacology), Quinolines (therapeutic use), Signal Transduction, TOR Serine-Threonine Kinases (antagonists & inhibitors), TOR Serine-Threonine Kinases (metabolism), Tumor Burden (drug effects), Xenograft Model Antitumor Assays.
MESH :
- chemical , antagonists & inhibitors : Proto-Oncogene Proteins c-akt, TOR Serine-Threonine Kinases.
- chemical , metabolism : Proto-Oncogene Proteins c-akt, TOR Serine-Threonine Kinases.
- chemical , pharmacology : Chloroquine, Imidazoles, Quinolines.
- drug effects : Apoptosis, Autophagy, Cell Proliferation, Tumor Burden.
- drug therapy : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- pathology : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- chemical , therapeutic use : Chloroquine, Imidazoles, Quinolines.
- Animals, Cell Line, Tumor, Drug Synergism, Female, Humans, Mice, Mice, Nude, Signal Transduction, Xenograft Model Antitumor Assays.

Abstract

Autophagy is a cellular lysosomal degradation pathway essential for regulation of cell survival and death to maintain homeostasis. This process is negatively regulated by mammalian target of rapamycin (mTOR) signaling and often counteracts efficacy of certain cancer therapeutic agents. NVP-BEZ235 (BEZ235) is a novel, orally bioavailable dual PI3K/mTOR inhibitor that has exhibited promising activity against non-small cell lung cancer (NSCLC) in preclinical models. The current study focuses on evaluating the role of BEZ235 in regulating autophagy. BEZ235 was effective in inhibiting the growth of NSCLC cells including induction of apoptosis. It also potently induced the expression of type-II LC3, indicating induction of autophagy. When BEZ235 was used in combination with the lysosomal or autophagic inhibitor chloroquine (CQ), enhanced inhibitory effects on monolayer growth and colony formation of NSCLC cells was observed. In addition, enhanced induction of apoptosis was also detected in cells exposed to the combination of BEZ235 and CQ. Moreover, the combination of BEZ235 and CQ was more effective than each single agent alone in inhibiting the growth of NSCLC xenografts in nude mice. Thus, induction of autophagy by BEZ235 appears to be a survival mechanism that may counteract its anticancer effects. Based on these, we suggest a strategy to enhance BEZ235's anticancer efficacy by blockade of autophagy.

DOI: 10.4161/cbt.12.6.16397
PubMed: 21738008

Affiliations:

Links toward previous steps (curation, corpus...)

to stream PubMed, to step Corpus: 000378
to stream PubMed, to step Curation: 000378

Links to Exploration step

pubmed:21738008

Le document en format XML

<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Augmentation of NVP-BEZ235's anticancer activity against human lung cancer cells by blockage of autophagy.</title>
<author><name sortKey="Xu, Cheng Xiong" sort="Xu, Cheng Xiong" uniqKey="Xu C" first="Cheng-Xiong" last="Xu">Cheng-Xiong Xu</name>
<affiliation wicri:level="2"><nlm:affiliation>Emory University School of Medicine and Winship Cancer Institute, Atlanta, GA, USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Emory University School of Medicine and Winship Cancer Institute, Atlanta, GA</wicri:regionArea>
<placeName><region type="state">Géorgie (États-Unis)</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Zhao, Liqun" sort="Zhao, Liqun" uniqKey="Zhao L" first="Liqun" last="Zhao">Liqun Zhao</name>
</author>
<author><name sortKey="Yue, Ping" sort="Yue, Ping" uniqKey="Yue P" first="Ping" last="Yue">Ping Yue</name>
</author>
<author><name sortKey="Fang, Guofu" sort="Fang, Guofu" uniqKey="Fang G" first="Guofu" last="Fang">Guofu Fang</name>
</author>
<author><name sortKey="Tao, Hui" sort="Tao, Hui" uniqKey="Tao H" first="Hui" last="Tao">Hui Tao</name>
</author>
<author><name sortKey="Owonikoko, Taofeek K" sort="Owonikoko, Taofeek K" uniqKey="Owonikoko T" first="Taofeek K" last="Owonikoko">Taofeek K. Owonikoko</name>
</author>
<author><name sortKey="Ramalingam, Suresh S" sort="Ramalingam, Suresh S" uniqKey="Ramalingam S" first="Suresh S" last="Ramalingam">Suresh S. Ramalingam</name>
</author>
<author><name sortKey="Khuri, Fadlo R" sort="Khuri, Fadlo R" uniqKey="Khuri F" first="Fadlo R" last="Khuri">Fadlo R. Khuri</name>
</author>
<author><name sortKey="Sun, Shi Yong" sort="Sun, Shi Yong" uniqKey="Sun S" first="Shi-Yong" last="Sun">Shi-Yong Sun</name>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">PubMed</idno>
<date when="2011">2011</date>
<idno type="RBID">pubmed:21738008</idno>
<idno type="pmid">21738008</idno>
<idno type="doi">10.4161/cbt.12.6.16397</idno>
<idno type="wicri:Area/PubMed/Corpus">000378</idno>
<idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000378</idno>
<idno type="wicri:Area/PubMed/Curation">000378</idno>
<idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000378</idno>
<idno type="wicri:Area/PubMed/Checkpoint">000376</idno>
<idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000376</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en">Augmentation of NVP-BEZ235's anticancer activity against human lung cancer cells by blockage of autophagy.</title>
<author><name sortKey="Xu, Cheng Xiong" sort="Xu, Cheng Xiong" uniqKey="Xu C" first="Cheng-Xiong" last="Xu">Cheng-Xiong Xu</name>
<affiliation wicri:level="2"><nlm:affiliation>Emory University School of Medicine and Winship Cancer Institute, Atlanta, GA, USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Emory University School of Medicine and Winship Cancer Institute, Atlanta, GA</wicri:regionArea>
<placeName><region type="state">Géorgie (États-Unis)</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Zhao, Liqun" sort="Zhao, Liqun" uniqKey="Zhao L" first="Liqun" last="Zhao">Liqun Zhao</name>
</author>
<author><name sortKey="Yue, Ping" sort="Yue, Ping" uniqKey="Yue P" first="Ping" last="Yue">Ping Yue</name>
</author>
<author><name sortKey="Fang, Guofu" sort="Fang, Guofu" uniqKey="Fang G" first="Guofu" last="Fang">Guofu Fang</name>
</author>
<author><name sortKey="Tao, Hui" sort="Tao, Hui" uniqKey="Tao H" first="Hui" last="Tao">Hui Tao</name>
</author>
<author><name sortKey="Owonikoko, Taofeek K" sort="Owonikoko, Taofeek K" uniqKey="Owonikoko T" first="Taofeek K" last="Owonikoko">Taofeek K. Owonikoko</name>
</author>
<author><name sortKey="Ramalingam, Suresh S" sort="Ramalingam, Suresh S" uniqKey="Ramalingam S" first="Suresh S" last="Ramalingam">Suresh S. Ramalingam</name>
</author>
<author><name sortKey="Khuri, Fadlo R" sort="Khuri, Fadlo R" uniqKey="Khuri F" first="Fadlo R" last="Khuri">Fadlo R. Khuri</name>
</author>
<author><name sortKey="Sun, Shi Yong" sort="Sun, Shi Yong" uniqKey="Sun S" first="Shi-Yong" last="Sun">Shi-Yong Sun</name>
</author>
</analytic>
<series><title level="j">Cancer biology & therapy</title>
<idno type="eISSN">1555-8576</idno>
<imprint><date when="2011" type="published">2011</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term>
<term>Apoptosis (drug effects)</term>
<term>Autophagy (drug effects)</term>
<term>Carcinoma, Non-Small-Cell Lung (drug therapy)</term>
<term>Carcinoma, Non-Small-Cell Lung (pathology)</term>
<term>Cell Line, Tumor</term>
<term>Cell Proliferation (drug effects)</term>
<term>Chloroquine (pharmacology)</term>
<term>Chloroquine (therapeutic use)</term>
<term>Drug Synergism</term>
<term>Female</term>
<term>Humans</term>
<term>Imidazoles (pharmacology)</term>
<term>Imidazoles (therapeutic use)</term>
<term>Lung Neoplasms (drug therapy)</term>
<term>Lung Neoplasms (pathology)</term>
<term>Mice</term>
<term>Mice, Nude</term>
<term>Proto-Oncogene Proteins c-akt (antagonists & inhibitors)</term>
<term>Proto-Oncogene Proteins c-akt (metabolism)</term>
<term>Quinolines (pharmacology)</term>
<term>Quinolines (therapeutic use)</term>
<term>Signal Transduction</term>
<term>TOR Serine-Threonine Kinases (antagonists & inhibitors)</term>
<term>TOR Serine-Threonine Kinases (metabolism)</term>
<term>Tumor Burden (drug effects)</term>
<term>Xenograft Model Antitumor Assays</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term>
<term>Apoptose ()</term>
<term>Autophagie ()</term>
<term>Carcinome pulmonaire non à petites cellules (anatomopathologie)</term>
<term>Carcinome pulmonaire non à petites cellules (traitement médicamenteux)</term>
<term>Charge tumorale ()</term>
<term>Chloroquine (pharmacologie)</term>
<term>Chloroquine (usage thérapeutique)</term>
<term>Femelle</term>
<term>Humains</term>
<term>Imidazoles (pharmacologie)</term>
<term>Imidazoles (usage thérapeutique)</term>
<term>Lignée cellulaire tumorale</term>
<term>Prolifération cellulaire ()</term>
<term>Protéines proto-oncogènes c-akt (antagonistes et inhibiteurs)</term>
<term>Protéines proto-oncogènes c-akt (métabolisme)</term>
<term>Quinoléines (pharmacologie)</term>
<term>Quinoléines (usage thérapeutique)</term>
<term>Souris</term>
<term>Souris nude</term>
<term>Synergie des médicaments</term>
<term>Sérine-thréonine kinases TOR (antagonistes et inhibiteurs)</term>
<term>Sérine-thréonine kinases TOR (métabolisme)</term>
<term>Tests d'activité antitumorale sur modèle de xénogreffe</term>
<term>Transduction du signal</term>
<term>Tumeurs du poumon (anatomopathologie)</term>
<term>Tumeurs du poumon (traitement médicamenteux)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Proto-Oncogene Proteins c-akt</term>
<term>TOR Serine-Threonine Kinases</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Proto-Oncogene Proteins c-akt</term>
<term>TOR Serine-Threonine Kinases</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Chloroquine</term>
<term>Imidazoles</term>
<term>Quinolines</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Carcinome pulmonaire non à petites cellules</term>
<term>Tumeurs du poumon</term>
</keywords>
<keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Protéines proto-oncogènes c-akt</term>
<term>Sérine-thréonine kinases TOR</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term>
<term>Autophagy</term>
<term>Cell Proliferation</term>
<term>Tumor Burden</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Carcinoma, Non-Small-Cell Lung</term>
<term>Lung Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Protéines proto-oncogènes c-akt</term>
<term>Sérine-thréonine kinases TOR</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Carcinoma, Non-Small-Cell Lung</term>
<term>Lung Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Chloroquine</term>
<term>Imidazoles</term>
<term>Quinoléines</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Chloroquine</term>
<term>Imidazoles</term>
<term>Quinolines</term>
</keywords>
<keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Carcinome pulmonaire non à petites cellules</term>
<term>Tumeurs du poumon</term>
</keywords>
<keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr"><term>Chloroquine</term>
<term>Imidazoles</term>
<term>Quinoléines</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Cell Line, Tumor</term>
<term>Drug Synergism</term>
<term>Female</term>
<term>Humans</term>
<term>Mice</term>
<term>Mice, Nude</term>
<term>Signal Transduction</term>
<term>Xenograft Model Antitumor Assays</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Apoptose</term>
<term>Autophagie</term>
<term>Charge tumorale</term>
<term>Femelle</term>
<term>Humains</term>
<term>Lignée cellulaire tumorale</term>
<term>Prolifération cellulaire</term>
<term>Souris</term>
<term>Souris nude</term>
<term>Synergie des médicaments</term>
<term>Tests d'activité antitumorale sur modèle de xénogreffe</term>
<term>Transduction du signal</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Autophagy is a cellular lysosomal degradation pathway essential for regulation of cell survival and death to maintain homeostasis. This process is negatively regulated by mammalian target of rapamycin (mTOR) signaling and often counteracts efficacy of certain cancer therapeutic agents. NVP-BEZ235 (BEZ235) is a novel, orally bioavailable dual PI3K/mTOR inhibitor that has exhibited promising activity against non-small cell lung cancer (NSCLC) in preclinical models. The current study focuses on evaluating the role of BEZ235 in regulating autophagy. BEZ235 was effective in inhibiting the growth of NSCLC cells including induction of apoptosis. It also potently induced the expression of type-II LC3, indicating induction of autophagy. When BEZ235 was used in combination with the lysosomal or autophagic inhibitor chloroquine (CQ), enhanced inhibitory effects on monolayer growth and colony formation of NSCLC cells was observed. In addition, enhanced induction of apoptosis was also detected in cells exposed to the combination of BEZ235 and CQ. Moreover, the combination of BEZ235 and CQ was more effective than each single agent alone in inhibiting the growth of NSCLC xenografts in nude mice. Thus, induction of autophagy by BEZ235 appears to be a survival mechanism that may counteract its anticancer effects. Based on these, we suggest a strategy to enhance BEZ235's anticancer efficacy by blockade of autophagy.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">21738008</PMID>
<DateCompleted><Year>2012</Year>
<Month>01</Month>
<Day>19</Day>
</DateCompleted>
<DateRevised><Year>2018</Year>
<Month>11</Month>
<Day>13</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1555-8576</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>12</Volume>
<Issue>6</Issue>
<PubDate><Year>2011</Year>
<Month>Sep</Month>
<Day>15</Day>
</PubDate>
</JournalIssue>
<Title>Cancer biology & therapy</Title>
<ISOAbbreviation>Cancer Biol. Ther.</ISOAbbreviation>
</Journal>
<ArticleTitle>Augmentation of NVP-BEZ235's anticancer activity against human lung cancer cells by blockage of autophagy.</ArticleTitle>
<Pagination><MedlinePgn>549-55</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.4161/cbt.12.6.16397</ELocationID>
<Abstract><AbstractText>Autophagy is a cellular lysosomal degradation pathway essential for regulation of cell survival and death to maintain homeostasis. This process is negatively regulated by mammalian target of rapamycin (mTOR) signaling and often counteracts efficacy of certain cancer therapeutic agents. NVP-BEZ235 (BEZ235) is a novel, orally bioavailable dual PI3K/mTOR inhibitor that has exhibited promising activity against non-small cell lung cancer (NSCLC) in preclinical models. The current study focuses on evaluating the role of BEZ235 in regulating autophagy. BEZ235 was effective in inhibiting the growth of NSCLC cells including induction of apoptosis. It also potently induced the expression of type-II LC3, indicating induction of autophagy. When BEZ235 was used in combination with the lysosomal or autophagic inhibitor chloroquine (CQ), enhanced inhibitory effects on monolayer growth and colony formation of NSCLC cells was observed. In addition, enhanced induction of apoptosis was also detected in cells exposed to the combination of BEZ235 and CQ. Moreover, the combination of BEZ235 and CQ was more effective than each single agent alone in inhibiting the growth of NSCLC xenografts in nude mice. Thus, induction of autophagy by BEZ235 appears to be a survival mechanism that may counteract its anticancer effects. Based on these, we suggest a strategy to enhance BEZ235's anticancer efficacy by blockade of autophagy.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Xu</LastName>
<ForeName>Cheng-Xiong</ForeName>
<Initials>CX</Initials>
<AffiliationInfo><Affiliation>Emory University School of Medicine and Winship Cancer Institute, Atlanta, GA, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhao</LastName>
<ForeName>Liqun</ForeName>
<Initials>L</Initials>
</Author>
<Author ValidYN="Y"><LastName>Yue</LastName>
<ForeName>Ping</ForeName>
<Initials>P</Initials>
</Author>
<Author ValidYN="Y"><LastName>Fang</LastName>
<ForeName>Guofu</ForeName>
<Initials>G</Initials>
</Author>
<Author ValidYN="Y"><LastName>Tao</LastName>
<ForeName>Hui</ForeName>
<Initials>H</Initials>
</Author>
<Author ValidYN="Y"><LastName>Owonikoko</LastName>
<ForeName>Taofeek K</ForeName>
<Initials>TK</Initials>
</Author>
<Author ValidYN="Y"><LastName>Ramalingam</LastName>
<ForeName>Suresh S</ForeName>
<Initials>SS</Initials>
</Author>
<Author ValidYN="Y"><LastName>Khuri</LastName>
<ForeName>Fadlo R</ForeName>
<Initials>FR</Initials>
</Author>
<Author ValidYN="Y"><LastName>Sun</LastName>
<ForeName>Shi-Yong</ForeName>
<Initials>SY</Initials>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>K23 CA164015</GrantID>
<Acronym>CA</Acronym>
<Agency>NCI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>P01 CA116676</GrantID>
<Acronym>CA</Acronym>
<Agency>NCI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 CA118450</GrantID>
<Acronym>CA</Acronym>
<Agency>NCI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
</GrantList>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2011</Year>
<Month>09</Month>
<Day>15</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>Cancer Biol Ther</MedlineTA>
<NlmUniqueID>101137842</NlmUniqueID>
<ISSNLinking>1538-4047</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D007093">Imidazoles</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D011804">Quinolines</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>886U3H6UFF</RegistryNumber>
<NameOfSubstance UI="D002738">Chloroquine</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber>
<NameOfSubstance UI="C546842">MTOR protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber>
<NameOfSubstance UI="D058570">TOR Serine-Threonine Kinases</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber>
<NameOfSubstance UI="D051057">Proto-Oncogene Proteins c-akt</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>RUJ6Z9Y0DT</RegistryNumber>
<NameOfSubstance UI="C531198">dactolisib</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002289" MajorTopicYN="N">Carcinoma, Non-Small-Cell Lung</DescriptorName>
<QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D045744" MajorTopicYN="N">Cell Line, Tumor</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D049109" MajorTopicYN="N">Cell Proliferation</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002738" MajorTopicYN="N">Chloroquine</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
<QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004357" MajorTopicYN="N">Drug Synergism</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D007093" MajorTopicYN="N">Imidazoles</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName>
<QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008175" MajorTopicYN="N">Lung Neoplasms</DescriptorName>
<QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008819" MajorTopicYN="N">Mice, Nude</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051057" MajorTopicYN="N">Proto-Oncogene Proteins c-akt</DescriptorName>
<QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D011804" MajorTopicYN="N">Quinolines</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName>
<QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D058570" MajorTopicYN="N">TOR Serine-Threonine Kinases</DescriptorName>
<QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D047368" MajorTopicYN="N">Tumor Burden</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D023041" MajorTopicYN="N">Xenograft Model Antitumor Assays</DescriptorName>
</MeshHeading>
</MeshHeadingList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2011</Year>
<Month>7</Month>
<Day>9</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed"><Year>2011</Year>
<Month>7</Month>
<Day>9</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2012</Year>
<Month>1</Month>
<Day>20</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">21738008</ArticleId>
<ArticleId IdType="pii">16397</ArticleId>
<ArticleId IdType="doi">10.4161/cbt.12.6.16397</ArticleId>
<ArticleId IdType="pmc">PMC3218593</ArticleId>
</ArticleIdList>
<ReferenceList><Reference><Citation>Science. 2002 Feb 1;295(5556):868-72</Citation>
<ArticleIdList><ArticleId IdType="pubmed">11786607</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Br J Cancer. 2008 Sep 2;99(5):683-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">18728656</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cancer Cell. 2003 Nov;4(5):343-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">14667501</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cancer Cell. 2004 Jul;6(1):91-9</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15261145</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Oncogene. 1992 Jan;7(1):171-80</Citation>
<ArticleIdList><ArticleId IdType="pubmed">1311061</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cancer Res. 1997 Nov 1;57(21):4931-9</Citation>
<ArticleIdList><ArticleId IdType="pubmed">9354460</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Oncogene. 1999 Apr 8;18(14):2357-65</Citation>
<ArticleIdList><ArticleId IdType="pubmed">10327056</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Natl Cancer Inst. 2004 Dec 1;96(23):1769-80</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15572759</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cancer Res. 2005 Apr 15;65(8):3336-46</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15833867</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Clin Invest. 2005 Oct;115(10):2679-88</Citation>
<ArticleIdList><ArticleId IdType="pubmed">16200202</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Curr Med Chem Anticancer Agents. 2005 Nov;5(6):575-89</Citation>
<ArticleIdList><ArticleId IdType="pubmed">16305480</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nat Rev Drug Discov. 2005 Dec;4(12):988-1004</Citation>
<ArticleIdList><ArticleId IdType="pubmed">16341064</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nature. 2006 May 25;441(7092):424-30</Citation>
<ArticleIdList><ArticleId IdType="pubmed">16724053</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nat Rev Drug Discov. 2007 Apr;6(4):304-12</Citation>
<ArticleIdList><ArticleId IdType="pubmed">17396135</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cell. 2008 Jan 11;132(1):27-42</Citation>
<ArticleIdList><ArticleId IdType="pubmed">18191218</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nature. 2008 Feb 28;451(7182):1069-75</Citation>
<ArticleIdList><ArticleId IdType="pubmed">18305538</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Drug Resist Updat. 2008 Feb-Apr;11(1-2):32-50</Citation>
<ArticleIdList><ArticleId IdType="pubmed">18166498</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mol Cancer Ther. 2008 Jul;7(7):1851-63</Citation>
<ArticleIdList><ArticleId IdType="pubmed">18606717</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cancer Res. 2008 Oct 1;68(19):8022-30</Citation>
<ArticleIdList><ArticleId IdType="pubmed">18829560</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nature. 2008 Oct 23;455(7216):1069-75</Citation>
<ArticleIdList><ArticleId IdType="pubmed">18948947</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nat Med. 2008 Dec;14(12):1351-6</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19029981</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cancer Biol Ther. 2008 Dec;7(12):1952-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">18981735</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Cancer Res. 2009 Oct 1;69(19):7644-52</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19789349</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 2009 Nov 17;106(46):19503-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">19850869</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 2009 Dec 29;106(52):22299-304</Citation>
<ArticleIdList><ArticleId IdType="pubmed">20007781</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>CA Cancer J Clin. 2010 Sep-Oct;60(5):277-300</Citation>
<ArticleIdList><ArticleId IdType="pubmed">20610543</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Sci Signal. 2010;3(147):ra81</Citation>
<ArticleIdList><ArticleId IdType="pubmed">21062993</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Drug Resist Updat. 2002 Dec;5(6):234-48</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12531180</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
</PubmedData>
</pubmed>
<affiliations><list><country><li>États-Unis</li>
</country>
<region><li>Géorgie (États-Unis)</li>
</region>
</list>
<tree><noCountry><name sortKey="Fang, Guofu" sort="Fang, Guofu" uniqKey="Fang G" first="Guofu" last="Fang">Guofu Fang</name>
<name sortKey="Khuri, Fadlo R" sort="Khuri, Fadlo R" uniqKey="Khuri F" first="Fadlo R" last="Khuri">Fadlo R. Khuri</name>
<name sortKey="Owonikoko, Taofeek K" sort="Owonikoko, Taofeek K" uniqKey="Owonikoko T" first="Taofeek K" last="Owonikoko">Taofeek K. Owonikoko</name>
<name sortKey="Ramalingam, Suresh S" sort="Ramalingam, Suresh S" uniqKey="Ramalingam S" first="Suresh S" last="Ramalingam">Suresh S. Ramalingam</name>
<name sortKey="Sun, Shi Yong" sort="Sun, Shi Yong" uniqKey="Sun S" first="Shi-Yong" last="Sun">Shi-Yong Sun</name>
<name sortKey="Tao, Hui" sort="Tao, Hui" uniqKey="Tao H" first="Hui" last="Tao">Hui Tao</name>
<name sortKey="Yue, Ping" sort="Yue, Ping" uniqKey="Yue P" first="Ping" last="Yue">Ping Yue</name>
<name sortKey="Zhao, Liqun" sort="Zhao, Liqun" uniqKey="Zhao L" first="Liqun" last="Zhao">Liqun Zhao</name>
</noCountry>
<country name="États-Unis"><region name="Géorgie (États-Unis)"><name sortKey="Xu, Cheng Xiong" sort="Xu, Cheng Xiong" uniqKey="Xu C" first="Cheng-Xiong" last="Xu">Cheng-Xiong Xu</name>
</region>
</country>
</tree>
</affiliations>
</record>

Pour manipuler ce document sous Unix (Dilib)

EXPLOR_STEP=$WICRI_ROOT/Sante/explor/ChloroquineV1/Data/PubMed/Checkpoint

HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000376 | SxmlIndent | more

HfdSelect -h $EXPLOR_AREA/Data/PubMed/Checkpoint/biblio.hfd -nk 000376 | SxmlIndent | more

Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Sante
   |area=    ChloroquineV1
   |flux=    PubMed
   |étape=   Checkpoint
   |type=    RBID
   |clé=     pubmed:21738008
   |texte=   Augmentation of NVP-BEZ235's anticancer activity against human lung cancer cells by blockage of autophagy.
}}

Pour générer des pages wiki

HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Checkpoint/RBID.i   -Sk "pubmed:21738008" \
       | HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Checkpoint/biblio.hfd   \
       | NlmPubMed2Wicri -a ChloroquineV1

This area was generated with Dilib version V0.6.33.
Data generation: Wed Mar 25 22:43:59 2020. Site generation: Sun Jan 31 12:44:45 2021

	Serveur d'exploration Chloroquine
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.

Serveur d'exploration Chloroquine

Augmentation of NVP-BEZ235's anticancer activity against human lung cancer cells by blockage of autophagy.

Augmentation of NVP-BEZ235's anticancer activity against human lung cancer cells by blockage of autophagy.

Source :

Descripteurs français

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Links to Exploration step

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

Pour générer des pages wiki