期刊
INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY
卷 77, 期 -, 页码 80-90出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.biocel.2016.05.020
关键词
Autophagy; Apoptosis; Reactive oxygen species; Prostate cancer
资金
- National Science Foundation of China [81573334, 81272462]
- Natural Science Foundation of Zhejiang Province of China [LY14H310013]
- Science and Technology Planning Project of Guangdong Province of China [2015A020211017]
- Team Project of Natural Science Foundation of Guangdong Province of China [S2013030013315]
- Undergraduate Innovation and Entrepreneurship Training Project of Jinan University [CX15096]
- Guangdong Provincial Thousand-Hundred-Ten Talent Project
The interplay between autophagy and apoptosis response to chemotherapy is still a subject of intense debate in recent years. More efforts have focused on the regulation effects of apoptosis on autophagy, whereas how autophagy affects apoptosis remains poorly understood. In this study performed on prostate cancer cells, we investigated the role of autophagy in adriamycin-induced apoptosis, as well as the mechanisms mediating the effects of autophagy on apoptosis response to adriamycin (ADM). The results show that ADM not only inhibited cell viability and enhanced apoptosis, but also promoted autophagy via PI3K/Akt(T308)/mTOR signal pathway. Inhibition of autophagy by either pharmacological inhibitor chloroquine (CQ) or RNA interference of Atg5 increased ADM-induced apoptosis and enhanced the chemosensitivity of prostate cancer cells. Moreover, blockade of autophagy augmented reactive oxygen species (ROS) generation induced by ADM. Scavenging of ROS by antioxidant N-acetyl-cysteine (NAC) reversed the strengthened effects of CQ on ADM-induced apoptosis and rescued the cells from apoptosis. The results identified ROS as a potential mediator directing the modulation effects of the protective autophagy on apoptosis response to ADM. Suppression of the protective autophagy might provide a promising strategy to increase the anticancer efficacy of agents in the treatment of prostate cancer. (C) 2016 Elsevier Ltd. All rights reserved.
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