Autophagy‐Mediated Degradation of IAPs and c‐FLIPL Potentiates Apoptosis Induced by Combination of TRAIL and Chal‐24
Identifieur interne : 000E28 ( Main/Exploration ); précédent : 000E27; suivant : 000E29Autophagy‐Mediated Degradation of IAPs and c‐FLIPL Potentiates Apoptosis Induced by Combination of TRAIL and Chal‐24
Auteurs : Jennings Xu ; Xiuling Xu ; Shaoqing Shi [États-Unis, République populaire de Chine] ; Qiong Wang [États-Unis, République populaire de Chine] ; Bryanna Saxton ; Weiyang He [République populaire de Chine] ; Xin Gou [République populaire de Chine] ; Jun-Ho Jang [République populaire de Chine] ; Toru Nyunoya [République populaire de Chine] ; Xia Wang [République populaire de Chine] ; Chengguo Xing ; Lin Zhang [République populaire de Chine] ; Yong Lin [République populaire de Chine]Source :
- Journal of Cellular Biochemistry [ 0730-2312 ] ; 2016-05.
Abstract
Combination chemotherapy is an effective strategy for increasing anticancer efficacy, reducing side effects and alleviating drug resistance. Here we report that combination of the recently identified novel chalcone derivative, chalcone‐24 (Chal‐24), and TNF‐related apoptosis‐inducing ligand (TRAIL) significantly increases cytotoxicity in lung cancer cells. Chal‐24 treatment significantly enhanced TRAIL‐induced activation of caspase‐8 and caspase‐3, and the cytotoxicity induced by combination of these agents was effectively suppressed by the pan‐caspase inhibitor z‐VAD‐fmk. Chal‐24 and TRAIL combination suppressed expression of cellular FLICE (FADD‐like IL‐1β‐converting enzyme)‐inhibitory protein large (c‐FLIPL) and cellular inhibitor of apoptosis proteins (c‐IAPs), and ectopic expression of c‐FLIPL and c‐IAPs inhibited the potentiated cytotoxicity. In addition, TRAIL and Chal‐24 cooperatively activated autophagy. Suppression of autophagy effectively attenuated cytotoxicity induced by Chal‐24 and TRAIL combination, which was associated with attenuation of c‐FLIPL and c‐IAPs degradation. Altogether, these results suggest that Chal‐24 potentiates the anticancer activity of TRAIL through autophagy‐mediated degradation of c‐FLIPL and c‐IAPs, and that combination of Chal‐24 and TRAIL could be an effective approach in improving chemotherapy efficacy. J. Cell. Biochem. 117: 1136–1144, 2016. © 2015 Wiley Periodicals, Inc.
Url:
DOI: 10.1002/jcb.25397
Affiliations:
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Chine</country><wicri:regionArea>Laboratory of Molecular and Translational Medicine, West China Second University Hospital, Sichuan University, 610041, Chengdu</wicri:regionArea><wicri:noRegion>Chengdu</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Qiong" sort="Wang, Qiong" uniqKey="Wang Q" first="Qiong" last="Wang">Qiong Wang</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Nouveau-Mexique</region></placeName><wicri:cityArea>Molecular Biology and Lung Cancer Program, Lovelace Respiratory Research Institute, 87108, Albuquerque</wicri:cityArea></affiliation><affiliation wicri:level="1"><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>Laboratory of Molecular and Translational Medicine, West China Second University Hospital, Sichuan University, 610041, Chengdu</wicri:regionArea><wicri:noRegion>Chengdu</wicri:noRegion></affiliation></author><author><name 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from="1136">1136</biblScope><biblScope unit="page" to="1144">1144</biblScope><biblScope unit="page-count">9</biblScope><date type="published" when="2016-05">2016-05</date></imprint><idno type="ISSN">0730-2312</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0730-2312</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Combination chemotherapy is an effective strategy for increasing anticancer efficacy, reducing side effects and alleviating drug resistance. Here we report that combination of the recently identified novel chalcone derivative, chalcone‐24 (Chal‐24), and TNF‐related apoptosis‐inducing ligand (TRAIL) significantly increases cytotoxicity in lung cancer cells. Chal‐24 treatment significantly enhanced TRAIL‐induced activation of caspase‐8 and caspase‐3, and the cytotoxicity induced by combination of these agents was effectively suppressed by the pan‐caspase inhibitor z‐VAD‐fmk. Chal‐24 and TRAIL combination suppressed expression of cellular FLICE (FADD‐like IL‐1β‐converting enzyme)‐inhibitory protein large (c‐FLIPL) and cellular inhibitor of apoptosis proteins (c‐IAPs), and ectopic expression of c‐FLIPL and c‐IAPs inhibited the potentiated cytotoxicity. In addition, TRAIL and Chal‐24 cooperatively activated autophagy. Suppression of autophagy effectively attenuated cytotoxicity induced by Chal‐24 and TRAIL combination, which was associated with attenuation of c‐FLIPL and c‐IAPs degradation. Altogether, these results suggest that Chal‐24 potentiates the anticancer activity of TRAIL through autophagy‐mediated degradation of c‐FLIPL and c‐IAPs, and that combination of Chal‐24 and TRAIL could be an effective approach in improving chemotherapy efficacy. J. Cell. Biochem. 117: 1136–1144, 2016. © 2015 Wiley Periodicals, Inc.</div></front></TEI><affiliations><list><country><li>République populaire de Chine</li><li>États-Unis</li></country><region><li>Nouveau-Mexique</li></region></list><tree><noCountry><name sortKey="Saxton, Bryanna" sort="Saxton, Bryanna" uniqKey="Saxton B" first="Bryanna" last="Saxton">Bryanna Saxton</name><name sortKey="Xing, Chengguo" sort="Xing, Chengguo" uniqKey="Xing C" first="Chengguo" last="Xing">Chengguo Xing</name><name sortKey="Xu, Jennings" sort="Xu, Jennings" uniqKey="Xu J" first="Jennings" last="Xu">Jennings Xu</name><name sortKey="Xu, Xiuling" sort="Xu, Xiuling" uniqKey="Xu X" first="Xiuling" last="Xu">Xiuling Xu</name></noCountry><country name="États-Unis"><region name="Nouveau-Mexique"><name sortKey="Shi, Shaoqing" sort="Shi, Shaoqing" uniqKey="Shi S" first="Shaoqing" last="Shi">Shaoqing Shi</name></region><name sortKey="Wang, Qiong" sort="Wang, Qiong" uniqKey="Wang Q" first="Qiong" last="Wang">Qiong Wang</name></country><country name="République populaire de Chine"><noRegion><name sortKey="Shi, Shaoqing" sort="Shi, Shaoqing" uniqKey="Shi S" first="Shaoqing" last="Shi">Shaoqing Shi</name></noRegion><name sortKey="Gou, Xin" sort="Gou, Xin" uniqKey="Gou X" first="Xin" last="Gou">Xin Gou</name><name sortKey="He, Weiyang" sort="He, Weiyang" uniqKey="He W" first="Weiyang" last="He">Weiyang He</name><name sortKey="Jang, Jun O" sort="Jang, Jun O" uniqKey="Jang J" first="Jun-Ho" last="Jang">Jun-Ho Jang</name><name sortKey="Lin, Yong" sort="Lin, Yong" uniqKey="Lin Y" first="Yong" last="Lin">Yong Lin</name><name sortKey="Nyunoya, Toru" sort="Nyunoya, Toru" uniqKey="Nyunoya T" first="Toru" last="Nyunoya">Toru Nyunoya</name><name sortKey="Wang, Qiong" sort="Wang, Qiong" uniqKey="Wang Q" first="Qiong" last="Wang">Qiong Wang</name><name sortKey="Wang, Xia" sort="Wang, Xia" uniqKey="Wang X" first="Xia" last="Wang">Xia Wang</name><name sortKey="Zhang, Lin" sort="Zhang, Lin" uniqKey="Zhang L" first="Lin" last="Zhang">Lin Zhang</name><name sortKey="Zhang, Lin" sort="Zhang, Lin" uniqKey="Zhang L" first="Lin" last="Zhang">Lin Zhang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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