Mutant p53 and Cellular Stress Pathways: A Criminal Alliance That Promotes Cancer Progression
Identifieur interne : 000613 ( Main/Exploration ); précédent : 000612; suivant : 000614Mutant p53 and Cellular Stress Pathways: A Criminal Alliance That Promotes Cancer Progression
Auteurs : Gabriella D Razi [Italie] ; Mara Cirone [Italie]Source :
- Cancers [ 2072-6694 ] ; 2019.
Abstract
The capability of cancer cells to manage stress induced by hypoxia, nutrient shortage, acidosis, redox imbalance, loss of calcium homeostasis and exposure to drugs is a key factor to ensure cancer survival and chemoresistance. Among the protective mechanisms utilized by cancer cells to cope with stress a pivotal role is played by the activation of heat shock proteins (HSP) response, anti-oxidant response induced by nuclear factor erythroid 2-related factor 2 (NRF2), the hypoxia-inducible factor-1 (HIF-1), the unfolded protein response (UPR) and autophagy, cellular processes strictly interconnected. However, depending on the type, intensity or duration of cellular stress, the balance between pro-survival and pro-death pathways may change, and cell survival may be shifted into cell death. Mutations of p53 (mutp53), occurring in more than 50% of human cancers, may confer oncogenic gain-of-function (GOF) to the protein, mainly due to its stabilization and interaction with the above reported cellular pathways that help cancer cells to adapt to stress. This review will focus on the interplay of mutp53 with HSPs, NRF2, UPR, and autophagy and discuss how the manipulation of these interconnected processes may tip the balance towards cell death or survival, particularly in response to therapies.
Url:
DOI: 10.3390/cancers11050614
PubMed: 31052524
PubMed Central: 6563084
Affiliations:
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Elena National Cancer Institute, 00144 Rome, Italy</nlm:aff><country xml:lang="fr">Italie</country><wicri:regionArea>Department of Research, IRCCS Regina Elena National Cancer Institute, 00144 Rome</wicri:regionArea><placeName><settlement type="city">Rome</settlement><region nuts="2">Latium</region></placeName></affiliation></author><author><name sortKey="Cirone, Mara" sort="Cirone, Mara" uniqKey="Cirone M" first="Mara" last="Cirone">Mara Cirone</name><affiliation wicri:level="1"><nlm:aff id="af3-cancers-11-00614">Department of Experimental Medicine, “Sapienza” University of Rome, 00185 Rome, Italy</nlm:aff><country xml:lang="fr">Italie</country><wicri:regionArea>Department of Experimental Medicine, “Sapienza” University of Rome, 00185 Rome</wicri:regionArea><placeName><settlement type="city">Rome</settlement><region nuts="2">Latium</region></placeName></affiliation><affiliation wicri:level="1"><nlm:aff id="af4-cancers-11-00614">Laboratory Affiliated to Pasteur Institute, Italy-Foundation Cenci Bolognetti, 00161 Rome, Italy</nlm:aff><country xml:lang="fr">Italie</country><wicri:regionArea>Laboratory Affiliated to Pasteur Institute, Italy-Foundation Cenci Bolognetti, 00161 Rome</wicri:regionArea><placeName><settlement type="city">Rome</settlement><region nuts="2">Latium</region></placeName></affiliation></author></analytic><series><title level="j">Cancers</title><idno type="eISSN">2072-6694</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>The capability of cancer cells to manage stress induced by hypoxia, nutrient shortage, acidosis, redox imbalance, loss of calcium homeostasis and exposure to drugs is a key factor to ensure cancer survival and chemoresistance. Among the protective mechanisms utilized by cancer cells to cope with stress a pivotal role is played by the activation of heat shock proteins (HSP) response, anti-oxidant response induced by nuclear factor erythroid 2-related factor 2 (NRF2), the hypoxia-inducible factor-1 (HIF-1), the unfolded protein response (UPR) and autophagy, cellular processes strictly interconnected. However, depending on the type, intensity or duration of cellular stress, the balance between pro-survival and pro-death pathways may change, and cell survival may be shifted into cell death. Mutations of p53 (mutp53), occurring in more than 50% of human cancers, may confer oncogenic gain-of-function (GOF) to the protein, mainly due to its stabilization and interaction with the above reported cellular pathways that help cancer cells to adapt to stress. This review will focus on the interplay of mutp53 with HSPs, NRF2, UPR, and autophagy and discuss how the manipulation of these interconnected processes may tip the balance towards cell death or survival, particularly in response to therapies.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Vousden, K H" uniqKey="Vousden K">K.H. Vousden</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Reinhardt, H C" uniqKey="Reinhardt H">H.C. Reinhardt</name></author><author><name sortKey="Schumacher, B" uniqKey="Schumacher B">B. Schumacher</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Bykov, V J N" uniqKey="Bykov V">V.J.N. Bykov</name></author><author><name sortKey="Eriksson, S E" uniqKey="Eriksson S">S.E. Eriksson</name></author><author><name sortKey="Bianchi, J" uniqKey="Bianchi J">J. Bianchi</name></author><author><name sortKey="Wiman, K G" uniqKey="Wiman K">K.G. 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White</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Gurpinar, E" uniqKey="Gurpinar E">E. Gurpinar</name></author><author><name sortKey="Vousden, K H" uniqKey="Vousden K">K.H. Vousden</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Blandino, G" uniqKey="Blandino G">G. Blandino</name></author><author><name sortKey="Di Agostino, S" uniqKey="Di Agostino S">S. Di Agostino</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>Italie</li></country><region><li>Latium</li></region><settlement><li>Rome</li></settlement></list><tree><country name="Italie"><noRegion><name sortKey="D Razi, Gabriella" sort="D Razi, Gabriella" uniqKey="D Razi G" first="Gabriella" last="D Razi">Gabriella D Razi</name></noRegion><name sortKey="Cirone, Mara" sort="Cirone, Mara" uniqKey="Cirone M" first="Mara" last="Cirone">Mara Cirone</name><name sortKey="Cirone, Mara" sort="Cirone, Mara" uniqKey="Cirone M" first="Mara" last="Cirone">Mara Cirone</name><name sortKey="D Razi, Gabriella" sort="D Razi, Gabriella" uniqKey="D Razi G" first="Gabriella" last="D Razi">Gabriella D Razi</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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