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KLF4 functions as an activator of the androgen receptor through reciprocal feedback.
Siu, M-K; Suau, F; Chen, W-Y; Tsai, Y-C; Tsai, H-Y; Yeh, H-L; Liu, Y-N.
Afiliação
  • Siu MK; Program for Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University and Academia Sinica, Taipei, Taiwan.
  • Suau F; Graduate Institute of Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan.
  • Chen WY; Department of Anesthesiology, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan.
  • Tsai YC; Department of Microbiology, Faculty of Pharmacy, Dicle University, Diyarbakir, Turkey.
  • Tsai HY; Department of Pathology, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan.
  • Yeh HL; Department of Pathology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
  • Liu YN; Program for Cancer Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University and Academia Sinica, Taipei, Taiwan.
Oncogenesis ; 5(12): e282, 2016 Dec 19.
Article em En | MEDLINE | ID: mdl-27991915
In prostate cancer, Krüppel-like factor 4 (KLF4) depletion occurs frequently, suggesting a role as suppressor tumor. KLF4 is a transcription factor associated with androgen receptor (AR) expression; however, its cellular functions and signaling regulation mechanism remain largely unknown. In this study, we demonstrated that activated AR binds to the KLF4 promoter and enhances KLF4 expression, which reciprocally targets the AR promoter, thus sustaining KLF4 activity. Ectopic KLF4 expression in androgen-independent prostate cancer cells induced AR expression and decreased cell proliferation, invasion and bone metastasis. We previously showed that increased microRNA (miR)-1 expression is associated with reduced bone metastasis of prostate cancer cells. Here we observed that KLF4 targets the primary miR-1-2 stem-loop promoter and stimulates miR-1 expression. In clinical prostate cancer specimens, KLF4 levels were positively correlated with miR-1 and AR levels. These data suggest that the loss of KLF4 expression is one mechanistic link between aggressive prostate cancer progression and low canonical AR output through miR-1 inactivation.

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Ano de publicação: 2016 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Ano de publicação: 2016 Tipo de documento: Article