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ZNF433 positively regulates the beta-catenin/TCF pathway in prostate cancer and enhances the tumorigenicity of cancer cells

Authors Gu S, Hou P, Liu K, Niu X, Wei B, Mao F, Xu Z

Received 25 June 2018

Accepted for publication 26 November 2018

Published 1 February 2019 Volume 2019:12 Pages 1031—1039

DOI https://doi.org/10.2147/OTT.S178150

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Andrew Yee

Peer reviewer comments 3

Editor who approved publication: Dr Sanjay Singh


Shuo Gu, Peijin Hou, Kun Liu, Xiaobing Niu, Bingjian Wei, Fei Mao, Zongyuan Xu

Department of Urology, Huai’an First People’s Hospital, Nanjing Medical University, Huai’an 223300, Jiangsu, People’s Republic of China

Background: Prostate cancer often shows the over-activation of beta-catenin/t-cell factor (TCF) signaling. It remains largely unknown how the beta-catenin/TCF transcriptional machinery is tightly controlled.
Methods: The ZNF433 mRNA and protein levels in the clinical tissues were examined using q-PCR, Western blot and immunohistochemistry. The phenotypes of prostate cancer cells were examined using MTT assay, Boyden chamber assay and anchorage-independent assay. The interaction between ZNF433 and beta-catenin was evaluated by immunoprecipitation.
Results: In the present study, ZNF433 was upregulated in prostate cancer samples, and promoted the growth and migration of prostate cancer cells. Furthermore, ZNF433 was the binding partner of beta-catenin and activated beta-catenin/TCF signaling in prostate cancer. Moreover, ZNF433 enhanced the binding between beta-catenin and TCF4. In addition, NC043, small antagonist for beta-catenin/TCF complex, inhibited the malignant behaviors of prostate cancer cells driven by ZNF433.
Conclusion: In summary, these studies demonstrate the tumor-promoting roles of ZNF433 in prostate cancer, and suggesting that ZNF433 was a potential target for the treatment.

Keywords: ZNF433, beta-catenin, prostate cancer, motility

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