Department of Oncology, Shanghai Tenth People's Hospital, Tongji University, Shanghai, 200072, PR China; Tongji University Cancer Center, Shanghai, 200072, PR China; Department of Oncology, Dermatology Hospital, Tongji University, Shanghai, 200443, PR China.
Department of Oncology, Shanghai Tenth People's Hospital, Tongji University, Shanghai, 200072, PR China; Tongji University Cancer Center, Shanghai, 200072, PR China; Department of Oncology, Dermatology Hospital, Tongji University, Shanghai, 200443, PR China.
Cancer Lett. 2018 Mar 1;416:24-30. doi: 10.1016/j.canlet.2017.12.013. Epub 2017 Dec 13.
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.
信号转导子和转录激活子 (STAT)3 的表达与肿瘤的生长、转移和预后相关；它还参与自噬的调节，而自噬可能反过来有助于肿瘤的化疗耐药性。然而，STAT3 是否参与癌细胞对化疗的存活反应尚不清楚。在这项研究中，我们表明自噬在化疗过程中被触发，并且抑制自噬增加了去势抵抗性前列腺癌 (CRPC) 细胞的化疗敏感性。同时，STAT3 的激活抑制了多西紫杉醇诱导的自噬，从而增加了线粒体损伤并降低了 CRPC 细胞活力。这些结果表明，STAT3 通过调节自噬促进 CRPC 细胞的存活和化疗耐药性。
