Regulation of Apoptosis by Autophagy to Enhance Cancer Therapy
Identifieur interne : 000475 ( Main/Exploration ); précédent : 000474; suivant : 000476Regulation of Apoptosis by Autophagy to Enhance Cancer Therapy
Auteurs : Kenneth D. Tompkins [États-Unis] ; Andrew Thorburn [États-Unis]Source :
- The Yale Journal of Biology and Medicine [ 0044-0086 ] ; 2019.
Abstract
In cancer therapy, a principle goal is to kill cancer cells while minimizing death of normal cells. Traditional cytotoxic therapies and the newer agents that target specific signaling proteins that are critical for cancer cell growth do this by activating a specific type of programmed cell death – apoptosis. However, it has been well established that cancer cells have varying levels of responses to apoptotic stimuli, with some being close to an “apoptotic threshold” and others being further away and that this ultimately determines whether cancer therapy is successful or not. In this review, we will highlight how the underlying mechanisms that control apoptosis thresholds relate to another important homeostatic process in cell survival and cell death, autophagy, and discuss recent evidence suggesting how inhibition of autophagy can enhance the action of anti-cancer drugs by modulating the apoptotic response.
Url:
PubMed: 31866785
PubMed Central: 6913805
Affiliations:
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Tompkins</name><affiliation wicri:level="2"><nlm:aff id="A1">Division of Endocrinology, Department of Medicine, University of Colorado School of Medicine, Aurora, CO</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Colorado</region></placeName><wicri:cityArea>Division of Endocrinology, Department of Medicine, University of Colorado School of Medicine, Aurora</wicri:cityArea></affiliation></author><author><name sortKey="Thorburn, Andrew" sort="Thorburn, Andrew" uniqKey="Thorburn A" first="Andrew" last="Thorburn">Andrew Thorburn</name><affiliation wicri:level="2"><nlm:aff id="A2">Department of Pharmacology, University of Colorado School of Medicine, Aurora, CO</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Colorado</region></placeName><wicri:cityArea>Department of Pharmacology, University of Colorado School of Medicine, Aurora</wicri:cityArea></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">31866785</idno><idno type="pmc">6913805</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6913805</idno><idno type="RBID">PMC:6913805</idno><date when="2019">2019</date><idno type="wicri:Area/Pmc/Corpus">000B19</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000B19</idno><idno type="wicri:Area/Pmc/Curation">000B19</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000B19</idno><idno type="wicri:Area/Pmc/Checkpoint">000431</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">000431</idno><idno type="wicri:Area/Ncbi/Merge">000D61</idno><idno type="wicri:Area/Ncbi/Curation">000D61</idno><idno type="wicri:Area/Ncbi/Checkpoint">000D61</idno><idno type="wicri:doubleKey">0044-0086:2019:Tompkins K:regulation:of:apoptosis</idno><idno type="wicri:Area/Main/Merge">000475</idno><idno type="wicri:Area/Main/Curation">000475</idno><idno type="wicri:Area/Main/Exploration">000475</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Regulation of Apoptosis by Autophagy to Enhance Cancer Therapy</title><author><name sortKey="Tompkins, Kenneth D" sort="Tompkins, Kenneth D" uniqKey="Tompkins K" first="Kenneth D." last="Tompkins">Kenneth D. Tompkins</name><affiliation wicri:level="2"><nlm:aff id="A1">Division of Endocrinology, Department of Medicine, University of Colorado School of Medicine, Aurora, CO</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Colorado</region></placeName><wicri:cityArea>Division of Endocrinology, Department of Medicine, University of Colorado School of Medicine, Aurora</wicri:cityArea></affiliation></author><author><name sortKey="Thorburn, Andrew" sort="Thorburn, Andrew" uniqKey="Thorburn A" first="Andrew" last="Thorburn">Andrew Thorburn</name><affiliation wicri:level="2"><nlm:aff id="A2">Department of Pharmacology, University of Colorado School of Medicine, Aurora, CO</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Colorado</region></placeName><wicri:cityArea>Department of Pharmacology, University of Colorado School of Medicine, Aurora</wicri:cityArea></affiliation></author></analytic><series><title level="j">The Yale Journal of Biology and Medicine</title><idno type="ISSN">0044-0086</idno><idno type="eISSN">1551-4056</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>In cancer therapy, a principle goal is to kill cancer cells while minimizing death of normal cells. Traditional cytotoxic therapies and the newer agents that target specific signaling proteins that are critical for cancer cell growth do this by activating a specific type of programmed cell death – apoptosis. However, it has been well established that cancer cells have varying levels of responses to apoptotic stimuli, with some being close to an “apoptotic threshold” and others being further away and that this ultimately determines whether cancer therapy is successful or not. In this review, we will highlight how the underlying mechanisms that control apoptosis thresholds relate to another important homeostatic process in cell survival and cell death, autophagy, and discuss recent evidence suggesting how inhibition of autophagy can enhance the action of anti-cancer drugs by modulating the apoptotic response.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Pistritto, G" uniqKey="Pistritto G">G Pistritto</name></author><author><name sortKey="Trisciuoglio, D" uniqKey="Trisciuoglio D">D Trisciuoglio</name></author><author><name sortKey="Ceci, C" uniqKey="Ceci C">C Ceci</name></author><author><name sortKey="Garufi, A" uniqKey="Garufi A">A Garufi</name></author><author><name sortKey="D Razi, G" uniqKey="D Razi G">G D’Orazi</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Yang, J" uniqKey="Yang J">J Yang</name></author><author><name sortKey="Zhao, H" uniqKey="Zhao H">H 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Andrysik</name></author><author><name sortKey="Hoh, M" uniqKey="Hoh M">M Hoh</name></author><author><name sortKey="Ludwig, M" uniqKey="Ludwig M">M Ludwig</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Warr, Mr" uniqKey="Warr M">MR Warr</name></author><author><name sortKey="Binnewies, M" uniqKey="Binnewies M">M Binnewies</name></author><author><name sortKey="Flach, J" uniqKey="Flach J">J Flach</name></author><author><name sortKey="Reynaud, D" uniqKey="Reynaud D">D Reynaud</name></author><author><name sortKey="Garg, T" uniqKey="Garg T">T Garg</name></author><author><name sortKey="Malhotra, R" uniqKey="Malhotra R">R Malhotra</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="You, H" uniqKey="You H">H You</name></author><author><name sortKey="Pellegrini, M" uniqKey="Pellegrini M">M Pellegrini</name></author><author><name sortKey="Tsuchihara, K" uniqKey="Tsuchihara K">K Tsuchihara</name></author><author><name sortKey="Yamamoto, K" uniqKey="Yamamoto K">K Yamamoto</name></author><author><name sortKey="Hacker, G" uniqKey="Hacker G">G Hacker</name></author><author><name sortKey="Erlacher, M" uniqKey="Erlacher M">M Erlacher</name></author></analytic></biblStruct><biblStruct></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Colorado</li></region></list><tree><country name="États-Unis"><region name="Colorado"><name sortKey="Tompkins, Kenneth D" sort="Tompkins, Kenneth D" uniqKey="Tompkins K" first="Kenneth D." last="Tompkins">Kenneth D. 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