CX4945 suppresses the growth of castration-resistant prostate cancer cells by reducing AR-V7 expression

CX4945 suppresses the growth of castration-resistant prostate cancer cells by reducing AR-V7... World J Urol (2017) 35:1213–1221 DOI 10.1007/s00345-016-1996-y ORIGINAL ARTICLE CX4945 suppresses the growth of castration-resistant prostate cancer cells by reducing AR-V7 expression 1,2,3 1,2,3 1,2,3 1,2,3 Chuangzhong Deng  · Jieping Chen  · Shengjie Guo  · Yanjun Wang  · 1,2,3 1,2,3 4 2,3,5 Qianghua Zhou  · Zaishang Li  · Xingping Yang  · Xingsu Yu  · 2,3,5 1,2,3 1,2,3 1,2,3 Zhenfeng Zhang  · Fangjian Zhou  · Hui Han  · Kai Yao   Received: 8 October 2016 / Accepted: 21 December 2016 / Published online: 19 January 2017 © Springer-Verlag Berlin Heidelberg 2017 Abstract assay. Protein and mRNA levels of full-length AR (AR-FL) Purpose The aberrant expression of casein kinase 2 and AR-V7 were determined by qPCR and western blot, (CK2) has been reported to be involved in the tumorigen- respectively. The nuclear translocation of p50 and p65 was esis and progression of prostate cancer. The inhibition of assessed to reflect the activity of the NF-κB pathway. CK2 activity represses androgen-dependent prostate cancer Results CX4945 reduced the proliferation of CRPC cells cells by attenuating the androgen receptor (AR) signaling in a dose-dependent and time-dependent manner. AR-V7 pathway. In this study, we examined the effect of CK2 inhi- rather than AR-FL was downregulated by CX4945 in both bition in castration-resistant prostate cancer (CRPC) cells, the mRNA and protein http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png World Journal of Urology Springer Journals

CX4945 suppresses the growth of castration-resistant prostate cancer cells by reducing AR-V7 expression

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Publisher
Springer Berlin Heidelberg
Copyright
Copyright © 2017 by Springer-Verlag Berlin Heidelberg
Subject
Medicine & Public Health; Urology; Nephrology; Oncology
ISSN
0724-4983
eISSN
1433-8726
D.O.I.
10.1007/s00345-016-1996-y
Publisher site
See Article on Publisher Site

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