Synergistic anticancer effect of cisplatin and Chal-24 combination through IAP and c-FLIPL degradation, Ripoptosome formation and autophagy-mediated apoptosis
Abstract
Drug resistance is a major hurdle in anticancer chemotherapy. Combined therapy using drugs with distinct mechanisms of function may increase anticancer efficacy. We have recently identified the novel chalcone derivative, chalcone-24 (Chal-24), as a potential therapeutic that kills cancer cells through activation of an autophagymediated necroptosis pathway. In this report, we investigated if Chal-24 can be combined with the frontline genotoxic anticancer drug, cisplatin for cancer therapy. The combination of Chal-24 and cisplatin synergistically induced apoptotic cytotoxicity in lung cancer cell lines, which was dependent on Chal-24-induced autophagy. While cisplatin slightly potentiated the JNK/Bcl2/Beclin1 pathway for autophagy activation, its combination with Chal-24 strongly triggered proteasomal degradation of the cellular inhibitor of apoptosis proteins (c-IAPs) and formation of the Ripoptosome complex that contains RIP1, FADD and caspase 8. Furthermore, the cisplatin and Chal-24 combination induced dramatic degradation of cellular FLICE (FADD-like IL-1β-converting enzyme)inhibitory protein large (cFLIPL) which suppresses Ripoptosome-mediated apoptosis activation. These results establish a novel mechanism for potentiation of anticancer activity with the combination of Chal-24 and cisplatin: to enhance apoptosis signaling through Ripoptosome formation and to release the apoptosis brake through c-FLIPL degradation. Altogether, our work suggests that the combination of Chal-24 and cisplatin could be employed to improvemore »
- Authors:
-
- Lovelace Biomedical and Environmental Research Institute, Albuquerque, NM (United States); Sichuan Univ., Chengdu (China)
- Lovelace Biomedical and Environmental Research Institute, Albuquerque, NM (United States)
- Lovelace Biomedical and Environmental Research Institute, Albuquerque, NM (United States); Univ. of New Mexico, Albuquerque, NM (United States)
- Department of Medicinal Chemistry, University of Minnesota, Minneapolis, MN, USA
- Sichuan Univ., Chengdu (China)
- Publication Date:
- Research Org.:
- Lovelace Biomedical and Environmental Research Institute, Albuquerque, NM (United States)
- Sponsoring Org.:
- USDOE Office of Science (SC), Biological and Environmental Research (BER); National Institutes of Health (NIH), National Institute of Environmental Health Sciences (NIEHS); NIH, National Cancer Institute (NCI); National Natural Science Foundation of China (NCFS)
- OSTI Identifier:
- 1627982
- Grant/Contract Number:
- SC0001173; R01ES017328; R01CA142649
- Resource Type:
- Accepted Manuscript
- Journal Name:
- Oncotarget
- Additional Journal Information:
- Journal Volume: 6; Journal Issue: 3; Journal ID: ISSN 1949-2553
- Publisher:
- Impact Journals
- Country of Publication:
- United States
- Language:
- English
- Subject:
- 60 APPLIED LIFE SCIENCES; Oncology; Cell Biology; autophagy; apoptosis; c-IAP; c-FLIP; cisplatin; Chal-24
Citation Formats
Shi, Shaoqing, Wang, Qiong, Xu, Jennings, Jang, Jun-Ho, Padilla, Mabel T., Nyunoya, Toru, Xing, Chengguo, Zhang, Lin, and Lin, Yong. Synergistic anticancer effect of cisplatin and Chal-24 combination through IAP and c-FLIPL degradation, Ripoptosome formation and autophagy-mediated apoptosis. United States: N. p., 2015.
Web. doi:10.18632/oncotarget.2746.
Shi, Shaoqing, Wang, Qiong, Xu, Jennings, Jang, Jun-Ho, Padilla, Mabel T., Nyunoya, Toru, Xing, Chengguo, Zhang, Lin, & Lin, Yong. Synergistic anticancer effect of cisplatin and Chal-24 combination through IAP and c-FLIPL degradation, Ripoptosome formation and autophagy-mediated apoptosis. United States. https://doi.org/10.18632/oncotarget.2746
Shi, Shaoqing, Wang, Qiong, Xu, Jennings, Jang, Jun-Ho, Padilla, Mabel T., Nyunoya, Toru, Xing, Chengguo, Zhang, Lin, and Lin, Yong. Fri .
"Synergistic anticancer effect of cisplatin and Chal-24 combination through IAP and c-FLIPL degradation, Ripoptosome formation and autophagy-mediated apoptosis". United States. https://doi.org/10.18632/oncotarget.2746. https://www.osti.gov/servlets/purl/1627982.
@article{osti_1627982,
title = {Synergistic anticancer effect of cisplatin and Chal-24 combination through IAP and c-FLIPL degradation, Ripoptosome formation and autophagy-mediated apoptosis},
author = {Shi, Shaoqing and Wang, Qiong and Xu, Jennings and Jang, Jun-Ho and Padilla, Mabel T. and Nyunoya, Toru and Xing, Chengguo and Zhang, Lin and Lin, Yong},
abstractNote = {Drug resistance is a major hurdle in anticancer chemotherapy. Combined therapy using drugs with distinct mechanisms of function may increase anticancer efficacy. We have recently identified the novel chalcone derivative, chalcone-24 (Chal-24), as a potential therapeutic that kills cancer cells through activation of an autophagymediated necroptosis pathway. In this report, we investigated if Chal-24 can be combined with the frontline genotoxic anticancer drug, cisplatin for cancer therapy. The combination of Chal-24 and cisplatin synergistically induced apoptotic cytotoxicity in lung cancer cell lines, which was dependent on Chal-24-induced autophagy. While cisplatin slightly potentiated the JNK/Bcl2/Beclin1 pathway for autophagy activation, its combination with Chal-24 strongly triggered proteasomal degradation of the cellular inhibitor of apoptosis proteins (c-IAPs) and formation of the Ripoptosome complex that contains RIP1, FADD and caspase 8. Furthermore, the cisplatin and Chal-24 combination induced dramatic degradation of cellular FLICE (FADD-like IL-1β-converting enzyme)inhibitory protein large (cFLIPL) which suppresses Ripoptosome-mediated apoptosis activation. These results establish a novel mechanism for potentiation of anticancer activity with the combination of Chal-24 and cisplatin: to enhance apoptosis signaling through Ripoptosome formation and to release the apoptosis brake through c-FLIPL degradation. Altogether, our work suggests that the combination of Chal-24 and cisplatin could be employed to improve chemotherapy efficacy.},
doi = {10.18632/oncotarget.2746},
journal = {Oncotarget},
number = 3,
volume = 6,
place = {United States},
year = {Fri Jan 30 00:00:00 EST 2015},
month = {Fri Jan 30 00:00:00 EST 2015}
}
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