Targeting Autophagy by MPT0L145, a Highly Potent PIK3C3 Inhibitor, Provides Synergistic Interaction to Targeted or Chemotherapeutic Agents in Cancer Cells
Identifieur interne : 000397 ( Main/Exploration ); précédent : 000396; suivant : 000398Targeting Autophagy by MPT0L145, a Highly Potent PIK3C3 Inhibitor, Provides Synergistic Interaction to Targeted or Chemotherapeutic Agents in Cancer Cells
Auteurs : Chun-Han Chen [Taïwan] ; Tsung-Han Hsieh [Taïwan] ; Yu-Chen Lin [Taïwan] ; Yun-Ru Liu [Taïwan] ; Jing-Ping Liou [Taïwan] ; Yun Yen [Taïwan]Source :
- Cancers [ 2072-6694 ] ; 2019.
Abstract
Anticancer therapies reportedly promote pro-survival autophagy in cancer cells that confers drug resistance, rationalizing the concept to combine autophagy inhibitors to increase their therapeutic potential. We previously identified that MPT0L145 is a PIK3C3/FGFR inhibitor that not only increases autophagosome formation due to fibroblast growth factor receptor (FGFR) inhibition but also perturbs autophagic flux via PIK3C3 inhibition in bladder cancer cells harboring FGFR activation. In this study, we hypothesized that combined-use of MPT0L145 with agents that induce pro-survival autophagy may provide synthetic lethality in cancer cells without FGFR activation. The results showed that MPT0L145 synergistically sensitizes anticancer effects of gefitinib and gemcitabine in non-small cell lung cancer A549 cells and pancreatic cancer PANC-1 cells, respectively. Mechanistically, drug combination increased incomplete autophagy due to impaired PIK3C3 function by MPT0L145 as evidenced by p62 accumulation and no additional apoptotic cell death was observed. Meanwhile, drug combination perturbed survival pathways and increased vacuolization and ROS production in cancer cells. In conclusion, the data suggest that halting pro-survival autophagy by targeting PIK3C3 with MPT0L145 significantly sensitizes cancer cells to targeted or chemotherapeutic agents, fostering rational combination strategies for cancer therapy in the future.
Url:
DOI: 10.3390/cancers11091345
PubMed: 31514441
PubMed Central: 6770340
Affiliations:
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Taiwan</nlm:aff><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Pharmacology, School of Medicine, College of Medicine, Taipei Medical University, Taipei 110</wicri:regionArea><wicri:noRegion>Taipei 110</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:aff id="af2-cancers-11-01345">Cell Physiology and Molecular Image Research Center, Wan Fang Hospital, Taipei Medical University, Taipei 110, Taiwan</nlm:aff><country xml:lang="fr">Taïwan</country><wicri:regionArea>Cell Physiology and Molecular Image Research Center, Wan Fang Hospital, Taipei Medical University, Taipei 110</wicri:regionArea><wicri:noRegion>Taipei 110</wicri:noRegion></affiliation></author><author><name sortKey="Hsieh, Tsung Han" sort="Hsieh, Tsung Han" uniqKey="Hsieh T" first="Tsung-Han" last="Hsieh">Tsung-Han Hsieh</name><affiliation wicri:level="1"><nlm:aff id="af3-cancers-11-01345">Joint Biobank, Office of Human Research, Taipei Medical University, Taipei 110, Taiwan</nlm:aff><country xml:lang="fr">Taïwan</country><wicri:regionArea>Joint Biobank, Office of Human Research, Taipei Medical University, Taipei 110</wicri:regionArea><wicri:noRegion>Taipei 110</wicri:noRegion></affiliation></author><author><name sortKey="Lin, Yu Chen" sort="Lin, Yu Chen" uniqKey="Lin Y" first="Yu-Chen" last="Lin">Yu-Chen Lin</name><affiliation wicri:level="1"><nlm:aff id="af1-cancers-11-01345">Department of Pharmacology, School of Medicine, College of Medicine, Taipei Medical University, Taipei 110, Taiwan</nlm:aff><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Pharmacology, School of Medicine, College of Medicine, Taipei Medical University, Taipei 110</wicri:regionArea><wicri:noRegion>Taipei 110</wicri:noRegion></affiliation></author><author><name sortKey="Liu, Yun Ru" sort="Liu, Yun Ru" uniqKey="Liu Y" first="Yun-Ru" last="Liu">Yun-Ru Liu</name><affiliation wicri:level="1"><nlm:aff id="af3-cancers-11-01345">Joint Biobank, Office of Human Research, Taipei Medical University, Taipei 110, Taiwan</nlm:aff><country xml:lang="fr">Taïwan</country><wicri:regionArea>Joint Biobank, Office of Human Research, Taipei Medical University, Taipei 110</wicri:regionArea><wicri:noRegion>Taipei 110</wicri:noRegion></affiliation></author><author><name sortKey="Liou, Jing Ping" sort="Liou, Jing Ping" uniqKey="Liou J" first="Jing-Ping" last="Liou">Jing-Ping Liou</name><affiliation wicri:level="1"><nlm:aff id="af4-cancers-11-01345">School of Pharmacy, College of Pharmacy, Taipei Medical University, Taipei 110, Taiwan</nlm:aff><country xml:lang="fr">Taïwan</country><wicri:regionArea>School of Pharmacy, College of Pharmacy, Taipei Medical University, Taipei 110</wicri:regionArea><wicri:noRegion>Taipei 110</wicri:noRegion></affiliation></author><author><name sortKey="Yen, Yun" sort="Yen, Yun" uniqKey="Yen Y" first="Yun" last="Yen">Yun Yen</name><affiliation wicri:level="1"><nlm:aff id="af5-cancers-11-01345">The Ph.D. Program for Cancer Molecular Biology and drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei 110, Taiwan</nlm:aff><country xml:lang="fr">Taïwan</country><wicri:regionArea>The Ph.D. Program for Cancer Molecular Biology and drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei 110</wicri:regionArea><wicri:noRegion>Taipei 110</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:aff id="af6-cancers-11-01345">TMU Research Center of Cancer Translational Medicine, Taipei Medical University Taipei 110, Taiwan</nlm:aff><country xml:lang="fr">Taïwan</country><wicri:regionArea>TMU Research Center of Cancer Translational Medicine, Taipei Medical University Taipei 110</wicri:regionArea><wicri:noRegion>Taipei Medical University Taipei 110</wicri:noRegion></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>Anticancer therapies reportedly promote pro-survival autophagy in cancer cells that confers drug resistance, rationalizing the concept to combine autophagy inhibitors to increase their therapeutic potential. We previously identified that MPT0L145 is a PIK3C3/FGFR inhibitor that not only increases autophagosome formation due to fibroblast growth factor receptor (FGFR) inhibition but also perturbs autophagic flux via PIK3C3 inhibition in bladder cancer cells harboring FGFR activation. In this study, we hypothesized that combined-use of MPT0L145 with agents that induce pro-survival autophagy may provide synthetic lethality in cancer cells without FGFR activation. The results showed that MPT0L145 synergistically sensitizes anticancer effects of gefitinib and gemcitabine in non-small cell lung cancer A549 cells and pancreatic cancer PANC-1 cells, respectively. Mechanistically, drug combination increased incomplete autophagy due to impaired PIK3C3 function by MPT0L145 as evidenced by p62 accumulation and no additional apoptotic cell death was observed. Meanwhile, drug combination perturbed survival pathways and increased vacuolization and ROS production in cancer cells. In conclusion, the data suggest that halting pro-survival autophagy by targeting PIK3C3 with MPT0L145 significantly sensitizes cancer cells to targeted or chemotherapeutic agents, fostering rational combination strategies for cancer therapy in the future.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Kaur, J" uniqKey="Kaur J">J. Kaur</name></author><author><name sortKey="Debnath, J" uniqKey="Debnath J">J. Debnath</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Boya, P" uniqKey="Boya P">P. Boya</name></author><author><name sortKey="Reggiori, F" uniqKey="Reggiori F">F. Reggiori</name></author><author><name sortKey="Codogno, P" uniqKey="Codogno P">P. Codogno</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Yang, J" uniqKey="Yang J">J. Yang</name></author><author><name sortKey="Carra, S" uniqKey="Carra S">S. 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Eliceiri</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>Taïwan</li></country></list><tree><country name="Taïwan"><noRegion><name sortKey="Chen, Chun Han" sort="Chen, Chun Han" uniqKey="Chen C" first="Chun-Han" last="Chen">Chun-Han Chen</name></noRegion><name sortKey="Chen, Chun Han" sort="Chen, Chun Han" uniqKey="Chen C" first="Chun-Han" last="Chen">Chun-Han Chen</name><name sortKey="Hsieh, Tsung Han" sort="Hsieh, Tsung Han" uniqKey="Hsieh T" first="Tsung-Han" last="Hsieh">Tsung-Han Hsieh</name><name sortKey="Lin, Yu Chen" sort="Lin, Yu Chen" uniqKey="Lin Y" first="Yu-Chen" last="Lin">Yu-Chen Lin</name><name sortKey="Liou, Jing Ping" sort="Liou, Jing Ping" uniqKey="Liou J" first="Jing-Ping" last="Liou">Jing-Ping Liou</name><name sortKey="Liu, Yun Ru" sort="Liu, Yun Ru" uniqKey="Liu Y" first="Yun-Ru" last="Liu">Yun-Ru Liu</name><name sortKey="Yen, Yun" sort="Yen, Yun" uniqKey="Yen Y" first="Yun" last="Yen">Yun Yen</name><name sortKey="Yen, Yun" sort="Yen, Yun" uniqKey="Yen Y" first="Yun" last="Yen">Yun Yen</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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