Axl Inhibitor R428 Enhances TRAIL-Mediated Apoptosis Through Downregulation of c-FLIP and Survivin Expression in Renal Carcinoma
Identifieur interne : 000A18 ( Main/Exploration ); précédent : 000A17; suivant : 000A19Axl Inhibitor R428 Enhances TRAIL-Mediated Apoptosis Through Downregulation of c-FLIP and Survivin Expression in Renal Carcinoma
Auteurs : Seon Min Woo [Corée du Sud] ; Kyoung-Jin Min [Corée du Sud] ; Seung Un Seo [Corée du Sud] ; Shin Kim [Corée du Sud] ; Peter Kubatka [Slovaquie] ; Jong-Wook Park [Corée du Sud] ; Taeg Kyu Kwon [Corée du Sud]Source :
- International Journal of Molecular Sciences [ 1422-0067 ] ; 2019.
Abstract
R428, a selective small molecule Axl inhibitor, is known to have anti-cancer effects, such as inhibition of invasion and proliferation and induction of cell death in cancer cells. The Axl receptor tyrosine kinase is highly expressed in cancer cells and the level of Axl expression is associated with survival, metastasis, and drug resistance of many cancer cells. However, the effect of Axl inhibition on overcoming anti-cancer drugs resistance is unclear. Therefore, we investigated the capability of Axl inhibition as a therapeutic agent for the induction of TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) sensitivity. In this study, R428 markedly sensitized cancer cells to TRAIL-induced apoptotic cell death, but not in normal human skin fibroblast (HSF) and human umbilical vein cells (EA.hy926). Moreover, knockdown of Axl by siRNA also increased TRAIL-induced apoptosis. R428 decreased c-FLIP proteins levels via induction of miR-708 expression and survivin protein levels at the post-translational level, and we found that knockdown of Axl also decreased both c-FLIP and survivin protein expression. Overexpression of c-FLIP and survivin markedly inhibited R428 plus TRAIL-induced apoptosis. Furthermore, R428 sensitized cancer cells to multiple anti-cancer drugs-mediated cell death. Our results provide that inhibition of Axl could improve sensitivity to TRAIL through downregulation of c-FLIP and survivin expression in renal carcinoma cells. Taken together, Axl may be a tempting target to overcome TRAIL resistance.
Url:
DOI: 10.3390/ijms20133253
PubMed: 31269715
PubMed Central: 6651098
Affiliations:
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Sud</country><wicri:regionArea>Department of Immunology, School of Medicine, Keimyung University, Daegu 42601</wicri:regionArea><wicri:noRegion>Daegu 42601</wicri:noRegion></affiliation></author><author><name sortKey="Min, Kyoung Jin" sort="Min, Kyoung Jin" uniqKey="Min K" first="Kyoung-Jin" last="Min">Kyoung-Jin Min</name><affiliation wicri:level="1"><nlm:aff id="af1-ijms-20-03253">Department of Immunology, School of Medicine, Keimyung University, Daegu 42601, Korea</nlm:aff><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Immunology, School of Medicine, Keimyung University, Daegu 42601</wicri:regionArea><wicri:noRegion>Daegu 42601</wicri:noRegion></affiliation></author><author><name sortKey="Seo, Seung Un" sort="Seo, Seung Un" uniqKey="Seo S" first="Seung Un" last="Seo">Seung Un Seo</name><affiliation wicri:level="1"><nlm:aff id="af1-ijms-20-03253">Department of Immunology, School of Medicine, Keimyung University, Daegu 42601, Korea</nlm:aff><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Immunology, School of Medicine, Keimyung University, Daegu 42601</wicri:regionArea><wicri:noRegion>Daegu 42601</wicri:noRegion></affiliation></author><author><name sortKey="Kim, Shin" sort="Kim, Shin" uniqKey="Kim S" first="Shin" last="Kim">Shin Kim</name><affiliation wicri:level="1"><nlm:aff id="af1-ijms-20-03253">Department of Immunology, School of Medicine, Keimyung University, Daegu 42601, Korea</nlm:aff><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Immunology, School of Medicine, Keimyung University, Daegu 42601</wicri:regionArea><wicri:noRegion>Daegu 42601</wicri:noRegion></affiliation></author><author><name sortKey="Kubatka, Peter" sort="Kubatka, Peter" uniqKey="Kubatka P" first="Peter" last="Kubatka">Peter Kubatka</name><affiliation wicri:level="1"><nlm:aff id="af2-ijms-20-03253">Department of Medical Biology, Jessenius Faculty of Medicine, Comenius University in Bratislava, 03601 Martin, Slovakia</nlm:aff><country xml:lang="fr">Slovaquie</country><wicri:regionArea>Department of Medical Biology, Jessenius Faculty of Medicine, Comenius University in Bratislava, 03601 Martin</wicri:regionArea><wicri:noRegion>03601 Martin</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:aff id="af3-ijms-20-03253">Department of Experimental Carcinogenesis, Division of Oncology, Biomedical Center Martin, Jessenius Faculty of Medicine, Comenius University in Bratislava, 03601 Martin, Slovakia</nlm:aff><country xml:lang="fr">Slovaquie</country><wicri:regionArea>Department of Experimental Carcinogenesis, Division of Oncology, Biomedical Center Martin, Jessenius Faculty of Medicine, Comenius University in Bratislava, 03601 Martin</wicri:regionArea><wicri:noRegion>03601 Martin</wicri:noRegion></affiliation></author><author><name sortKey="Park, Jong Wook" sort="Park, Jong Wook" uniqKey="Park J" first="Jong-Wook" last="Park">Jong-Wook Park</name><affiliation wicri:level="1"><nlm:aff id="af1-ijms-20-03253">Department of Immunology, School of Medicine, Keimyung University, Daegu 42601, Korea</nlm:aff><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Immunology, School of Medicine, Keimyung University, Daegu 42601</wicri:regionArea><wicri:noRegion>Daegu 42601</wicri:noRegion></affiliation></author><author><name sortKey="Kwon, Taeg Kyu" sort="Kwon, Taeg Kyu" uniqKey="Kwon T" first="Taeg Kyu" last="Kwon">Taeg Kyu Kwon</name><affiliation wicri:level="1"><nlm:aff id="af1-ijms-20-03253">Department of Immunology, School of Medicine, Keimyung University, Daegu 42601, Korea</nlm:aff><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Immunology, School of Medicine, Keimyung University, Daegu 42601</wicri:regionArea><wicri:noRegion>Daegu 42601</wicri:noRegion></affiliation></author></analytic><series><title level="j">International Journal of Molecular Sciences</title><idno type="eISSN">1422-0067</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>R428, a selective small molecule Axl inhibitor, is known to have anti-cancer effects, such as inhibition of invasion and proliferation and induction of cell death in cancer cells. The Axl receptor tyrosine kinase is highly expressed in cancer cells and the level of Axl expression is associated with survival, metastasis, and drug resistance of many cancer cells. However, the effect of Axl inhibition on overcoming anti-cancer drugs resistance is unclear. Therefore, we investigated the capability of Axl inhibition as a therapeutic agent for the induction of TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) sensitivity. In this study, R428 markedly sensitized cancer cells to TRAIL-induced apoptotic cell death, but not in normal human skin fibroblast (HSF) and human umbilical vein cells (EA.hy926). Moreover, knockdown of Axl by siRNA also increased TRAIL-induced apoptosis. R428 decreased c-FLIP proteins levels via induction of miR-708 expression and survivin protein levels at the post-translational level, and we found that knockdown of Axl also decreased both c-FLIP and survivin protein expression. Overexpression of c-FLIP and survivin markedly inhibited R428 plus TRAIL-induced apoptosis. Furthermore, R428 sensitized cancer cells to multiple anti-cancer drugs-mediated cell death. Our results provide that inhibition of Axl could improve sensitivity to TRAIL through downregulation of c-FLIP and survivin expression in renal carcinoma cells. Taken together, Axl may be a tempting target to overcome TRAIL resistance.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Almasan, A" uniqKey="Almasan A">A. Almasan</name></author><author><name sortKey="Ashkenazi, A" uniqKey="Ashkenazi A">A. Ashkenazi</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Johnstone, R W" uniqKey="Johnstone R">R.W. Johnstone</name></author><author><name sortKey="Frew, A J" uniqKey="Frew A">A.J. Frew</name></author><author><name sortKey="Smyth, M J" uniqKey="Smyth M">M.J. 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Kwon</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>Corée du Sud</li><li>Slovaquie</li></country></list><tree><country name="Corée du Sud"><noRegion><name sortKey="Woo, Seon Min" sort="Woo, Seon Min" uniqKey="Woo S" first="Seon Min" last="Woo">Seon Min Woo</name></noRegion><name sortKey="Kim, Shin" sort="Kim, Shin" uniqKey="Kim S" first="Shin" last="Kim">Shin Kim</name><name sortKey="Kwon, Taeg Kyu" sort="Kwon, Taeg Kyu" uniqKey="Kwon T" first="Taeg Kyu" last="Kwon">Taeg Kyu Kwon</name><name sortKey="Min, Kyoung Jin" sort="Min, Kyoung Jin" uniqKey="Min K" first="Kyoung-Jin" last="Min">Kyoung-Jin Min</name><name sortKey="Park, Jong Wook" sort="Park, Jong Wook" uniqKey="Park J" first="Jong-Wook" last="Park">Jong-Wook Park</name><name sortKey="Seo, Seung Un" sort="Seo, Seung Un" uniqKey="Seo S" first="Seung Un" last="Seo">Seung Un Seo</name></country><country name="Slovaquie"><noRegion><name sortKey="Kubatka, Peter" sort="Kubatka, Peter" uniqKey="Kubatka P" first="Peter" last="Kubatka">Peter Kubatka</name></noRegion><name sortKey="Kubatka, Peter" sort="Kubatka, Peter" uniqKey="Kubatka P" first="Peter" last="Kubatka">Peter Kubatka</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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