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Title: Wnt signaling promotes androgen-independent prostate cancer cell proliferation through up-regulation of the hippo pathway effector YAP

Journal Article · · Biochemical and Biophysical Research Communications
 [1];  [2]; ;  [3];  [1];  [4];  [2]
  1. Department of Urology, Busan Paik Hospital, Inje University 633-165, Busan 47392 (Korea, Republic of)
  2. Department of Bio and Fermentation Convergence Technology, Kookmin University, BK21 PLUS Program, Seoul 02707 (Korea, Republic of)
  3. Department of Life Science, Sogang University, Seoul 04107 (Korea, Republic of)
  4. Department of Urology, Kosin University Gospel Hospital, Busan (Korea, Republic of)

Aberrant up-regulation of Wnt/β-catenin signaling is associated with the development and progression of prostate cancer, but the underlying mechanism is unclear. Here we show that in the absence of androgens, the Wnt/β-catenin pathway activates AR-mediated transcription through up-regulation of the Hippo pathway effector Yes-associated protein (YAP). Wnt3a-conditioned medium (Wnt3a-CM) promotes the growth of LNCaP cells and increases AR and YAP protein levels. Moreover, Wnt3a-CM induces the nuclear translocation of YAP and the AR, but not β-catenin, thereby activating the expression of AR- and YAP-dependent genes, in an androgen-independent manner. In addition, depletion of YAP with small interfering RNA (siRNA) prevented Wnt3a-CM-mediated up-regulation of AR-dependent gene expression. Thus, our findings provide mechanistic insight into the proposed cross-talk between the Wnt/β-catenin and Hippo pathways in androgen-independent prostate cancer development. - Highlights: • Wnt3a promotes androgen-independent prostate cancer cell growth. • Wnt3a activates YAP- and AR-mediated transcription in the absence of androgen. • YAP is required for Wnt3a-induced AR activation in the absence of androgen.

OSTI ID:
22697011
Journal Information:
Biochemical and Biophysical Research Communications, Vol. 486, Issue 4; Other Information: Copyright (c) 2017 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
Country of Publication:
United States
Language:
English