The pharmalogical reactivation of p53 function improves breast tumor cell lysis by granzyme B and NK cells through induction of autophagy
Identifieur interne : 000027 ( France/Analysis ); précédent : 000026; suivant : 000028The pharmalogical reactivation of p53 function improves breast tumor cell lysis by granzyme B and NK cells through induction of autophagy
Auteurs : Marie Chollat-Namy [France] ; Thouraya Ben Safta-Saadoun [France] ; Djazia Haferssas [France] ; Guillaume Meurice [France] ; Salem Chouaib [France, Émirats arabes unis] ; Jerome Thiery [France]Source :
- Cell Death & Disease [ 2041-4889 ] ; 2019.
Abstract
Cytotoxic T lymphocytes (CTL) and natural killer cells (NK)-mediated elimination of tumor cells is mostly dependent on Granzyme B apoptotic pathway, which is regulated by the wild type (wt) p53 protein. Because
Url:
DOI: 10.1038/s41419-019-1950-1
PubMed: 31541080
PubMed Central: 6754511
Affiliations:
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PMC:6754511Le document en format XML
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of Precision Medicine,</institution><institution>Gulf Medical University,</institution></institution-wrap>Ajman, United Arab Emirates</nlm:aff><country xml:lang="fr">Émirats arabes unis</country><wicri:regionArea>Ajman</wicri:regionArea></affiliation></author><author><name sortKey="Thiery, Jerome" sort="Thiery, Jerome" uniqKey="Thiery J" first="Jerome" last="Thiery">Jerome Thiery</name><affiliation wicri:level="1"><nlm:aff id="Aff1">INSERM U1186, Villejuif, France</nlm:aff><country xml:lang="fr">France</country><wicri:regionArea>INSERM U1186, Villejuif</wicri:regionArea><wicri:noRegion>Villejuif</wicri:noRegion><wicri:noRegion>Villejuif</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:aff id="Aff2"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 2284 9388</institution-id><institution-id institution-id-type="GRID">grid.14925.3b</institution-id><institution>Gustave Roussy Cancer Campus,</institution></institution-wrap>Villejuif, France</nlm:aff><country xml:lang="fr">France</country><wicri:regionArea>Villejuif</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="Aff3"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 2171 2558</institution-id><institution-id institution-id-type="GRID">grid.5842.b</institution-id><institution>University Paris Sud, Faculty of Medicine,</institution></institution-wrap>Le Kremlin Bicêtre, France</nlm:aff><country xml:lang="fr">France</country><wicri:regionArea>Le Kremlin Bicêtre</wicri:regionArea></affiliation></author></analytic><series><title level="j">Cell Death & Disease</title><idno type="eISSN">2041-4889</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 id="Par1">Cytotoxic T lymphocytes (CTL) and natural killer cells (NK)-mediated elimination of tumor cells is mostly dependent on Granzyme B apoptotic pathway, which is regulated by the wild type (wt) p53 protein. Because <italic>TP53</italic> inactivating mutations, frequently found in human tumors, could interfere with Granzyme B-mediated cell death, the use of small molecules developed to reactivate wtp53 function in p53-mutated tumor cells could optimize their lysis by CTL or NK cells. Here, we show that the pharmalogical reactivation of a wt-like p53 function in p53-mutated breast cancer cells using the small molecule CP-31398 increases their sensitivity to NK-mediated lysis. This potentiation is dependent on p53-mediated induction of autophagy via the sestrin-AMPK-mTOR pathway and the ULK axis. This CP31398-induced autophagy sequestrates in autophagosomes several anti-apoptotic proteins, including Bcl-X<sub>L</sub> and XIAP, facilitating Granzyme B-mediated mitochondrial outer membrane permeabilization, caspase-3 activation and Granzyme B- or NK cell-induced apoptosis. Together, our results define a new way to increase cytotoxic lymphocyte-mediated lysis of p53-mutated breast cancer cell, through a p53-dependent autophagy induction, with potential applications in combined immunotherapeutic approaches.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Voskoboinik, I" uniqKey="Voskoboinik I">I Voskoboinik</name></author><author><name sortKey="Whisstock, Jc" uniqKey="Whisstock J">JC Whisstock</name></author><author><name sortKey="Trapani, Ja" uniqKey="Trapani J">JA Trapani</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Thiery, J" uniqKey="Thiery J">J Thiery</name></author><author><name sortKey="Safta, Tb" uniqKey="Safta T">TB Safta</name></author><author><name sortKey="Ziani, L" uniqKey="Ziani L">L Ziani</name></author><author><name sortKey="Chouaib, S" uniqKey="Chouaib S">S Chouaib</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Thiery, J" uniqKey="Thiery J">J Thiery</name></author><author><name sortKey="Lieberman, J" uniqKey="Lieberman J">J Lieberman</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Heibein, Jeffrey A" uniqKey="Heibein J">Jeffrey A. 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Krayem</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>France</li><li>Émirats arabes unis</li></country></list><tree><country name="France"><noRegion><name sortKey="Chollat Namy, Marie" sort="Chollat Namy, Marie" uniqKey="Chollat Namy M" first="Marie" last="Chollat-Namy">Marie Chollat-Namy</name></noRegion><name sortKey="Ben Safta Saadoun, Thouraya" sort="Ben Safta Saadoun, Thouraya" uniqKey="Ben Safta Saadoun T" first="Thouraya" last="Ben Safta-Saadoun">Thouraya Ben Safta-Saadoun</name><name sortKey="Ben Safta Saadoun, Thouraya" sort="Ben Safta Saadoun, Thouraya" uniqKey="Ben Safta Saadoun T" first="Thouraya" last="Ben Safta-Saadoun">Thouraya Ben Safta-Saadoun</name><name sortKey="Ben Safta Saadoun, Thouraya" sort="Ben Safta Saadoun, Thouraya" uniqKey="Ben Safta Saadoun T" first="Thouraya" last="Ben Safta-Saadoun">Thouraya Ben Safta-Saadoun</name><name sortKey="Chollat Namy, Marie" sort="Chollat Namy, Marie" uniqKey="Chollat Namy M" first="Marie" last="Chollat-Namy">Marie Chollat-Namy</name><name sortKey="Chollat Namy, Marie" sort="Chollat Namy, Marie" uniqKey="Chollat Namy M" first="Marie" last="Chollat-Namy">Marie Chollat-Namy</name><name sortKey="Chouaib, Salem" sort="Chouaib, Salem" uniqKey="Chouaib S" first="Salem" last="Chouaib">Salem Chouaib</name><name sortKey="Chouaib, Salem" sort="Chouaib, Salem" uniqKey="Chouaib S" first="Salem" last="Chouaib">Salem Chouaib</name><name sortKey="Chouaib, Salem" sort="Chouaib, Salem" uniqKey="Chouaib S" first="Salem" last="Chouaib">Salem Chouaib</name><name sortKey="Haferssas, Djazia" sort="Haferssas, Djazia" uniqKey="Haferssas D" first="Djazia" last="Haferssas">Djazia Haferssas</name><name sortKey="Haferssas, Djazia" sort="Haferssas, Djazia" uniqKey="Haferssas D" first="Djazia" last="Haferssas">Djazia Haferssas</name><name sortKey="Haferssas, Djazia" sort="Haferssas, Djazia" uniqKey="Haferssas D" first="Djazia" last="Haferssas">Djazia Haferssas</name><name sortKey="Meurice, Guillaume" sort="Meurice, Guillaume" uniqKey="Meurice G" first="Guillaume" last="Meurice">Guillaume Meurice</name><name sortKey="Thiery, Jerome" sort="Thiery, Jerome" uniqKey="Thiery J" first="Jerome" last="Thiery">Jerome Thiery</name><name sortKey="Thiery, Jerome" sort="Thiery, Jerome" uniqKey="Thiery J" first="Jerome" last="Thiery">Jerome Thiery</name><name sortKey="Thiery, Jerome" sort="Thiery, Jerome" uniqKey="Thiery J" first="Jerome" last="Thiery">Jerome Thiery</name></country><country name="Émirats arabes unis"><noRegion><name sortKey="Chouaib, Salem" sort="Chouaib, Salem" uniqKey="Chouaib S" first="Salem" last="Chouaib">Salem Chouaib</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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