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Autophagy-Mediated Degradation of IAPs and c-FLIP(L) Potentiates Apoptosis Induced by Combination of TRAIL and Chal-24.

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收录情况： ◇ SCIE

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机构： [1]Molecular Biology and Lung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, 87108, New Mexico. [2]Laboratory of Molecular and Translational Medicine, West China Second University Hospital, Sichuan University, Chengdu, 610041, P.R. China. [3]Department of Urology, The First Affiliated Hospital, Chongqing Medical University, Chongqing, 510182, P.R. China. [4]Division of Pulmonary and Critical Care Medicine, University of New Mexico and New Mexico VA Health Care System, Albuquerque, New Mexico. [5]Department of Medicinal Chemistry, University of Minnesota, Minneapolis, 55455, Minnesota.

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关键词： TRAIL CHAL-24 AUTOPHAGY APOPTOSIS c-IAP c-FLIP

摘要：

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-FLIP(L)) and cellular inhibitor of apoptosis proteins (c-IAPs), and ectopic expression of c-FLIP(L) 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-FLIP(L) and c-IAPs degradation. Altogether, these results suggest that Chal-24 potentiates the anticancer activity of TRAIL through autophagy-mediated degradation of c-FLIP(L) and c-IAPs, and that combination of Chal-24 and TRAIL could be an effective approach in improving chemotherapy efficacy. © 2015 Wiley Periodicals, Inc.

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出版当年[2016]版：

大类 | 2 区生物

小类 | 3 区生化与分子生物学 3 区细胞生物学

最新[2023]版：

大类 | 3 区生物学

小类 | 3 区生化与分子生物学 4 区细胞生物学

JCR分区：

出版当年[2016]版：

Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Q3 CELL BIOLOGY

最新[2023]版：

Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Q3 CELL BIOLOGY

影响因子： 3 最新[2023版] 3.1 最新五年平均 3.085 出版当年[2016版] 3.196 出版当年五年平均 3.446 出版前一年[2015版] 2.959 出版后一年[2017版]

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第一作者机构： [1]Molecular Biology and Lung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, 87108, New Mexico.

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通讯作者：

通讯机构： [1]Molecular Biology and Lung Cancer Program, Lovelace Respiratory Research Institute, Albuquerque, 87108, New Mexico. [2]Laboratory of Molecular and Translational Medicine, West China Second University Hospital, Sichuan University, Chengdu, 610041, P.R. China. [*1]Molecular Biology and Lung Cancer Program, Lovelace Respiratory Research Institute, 2425 Ridgecrest Dr., SE, Albuquerque, NM 87108. [*2]Laboratory of Molecular and Translational Medicine, West China Second University Hospital, Sichuan University, Chengdu 610041, China

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Autophagy-Mediated Degradation of IAPs and c-FLIP(L) Potentiates Apoptosis Induced by Combination of TRAIL and Chal-24.

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