Docetaxel-mediated autophagy promotes chemoresistance in castration-resistant prostate cancer cells by inhibiting STAT3.
Cancer Lett
; 416: 24-30, 2018 03 01.
Article
em En
| MEDLINE
| ID: mdl-29246644
ABSTRACT
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.
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Base de dados:
MEDLINE
Assunto principal:
Autofagia
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Resistencia a Medicamentos Antineoplásicos
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Taxoides
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Fator de Transcrição STAT3
Idioma:
En
Ano de publicação:
2018
Tipo de documento:
Article