期刊
CANCER LETTERS
卷 416, 期 -, 页码 24-30出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2017.12.013
关键词
Autophagy; Chemotherapy; STAT3; Castration-resistant prostate cancer
类别
资金
- National Natural Science Foundation of China [81372749, 81772905, 81702311]
- Shanghai Committee of Science and Technology, China [11411950602]
- Shanghai Health System Advanced Technology Promotion Project, China [2013SY046]
- Fundamental Research Funds for the Central Universities, China [1501219146]
Signal transducer and activator of transcription (STAT)3 expression is correlated with neoplasm growth, metastasis, and prognosis: it has also been implicated in the regulation of autophagy, which may in turn contribute to tumor chemoresistance. However, it is unknown whether STAT3 is involved in cancer cell survival in response to chemotherapy. In this study, we show that autophagy is triggered during chemotherapy and that inhibiting autophagy increased chemosensitivity of castration-resistant prostate cancer (CRPC) cells. Meanwhile, docetaxel induced autophagy was inhibited by STAT3 activation, which increased mitochondrial damage and decreased CRPC cell viability. These results suggest that STAT3 contributes to CRPC cell survival and chemoresistance by modulating autophagy. (C) 2017 Elsevier B.V. All rights reserved.
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