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PBOV1通过促进G1/S期转换来促进前列腺癌增殖。

PBOV1 promotes prostate cancer proliferation by promoting G1/S transition.

作者信息

Pan Tiejun, Wu Rongpei, Liu Bo, Wen Handong, Tu Zhong, Guo Jun, Yang Jiarong, Shen Guoqiu

机构信息

Department of Urology, Wuhan General Hospital of Guangzhou Military Command, Wuhan, Hubei, People's Republic of China.

Department of Urology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, People's Republic of China.

出版信息

Onco Targets Ther. 2016 Feb 16;9:787-95. doi: 10.2147/OTT.S92682. eCollection 2016.

DOI:10.2147/OTT.S92682
PMID:26937201
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4762445/
Abstract

Prostate cancer (PC) is one of the leading causes of cancer death in men, and thus, finding new regulators is critical for PC therapy. Prostate and breast cancer overexpressed 1 (PBOV1) is overexpressed in breast, prostate, and bladder cancers, as it is upregulated in the serum of patients with PC, but the role of PBOV1 in PC has not been studied. In this article, we found that PBOV1 was indeed overexpressed in PC cells; PBOV1 overexpression promoted cell proliferation and colony formation ability and arrested cell cycle in the G0/G1 phase and tumorigenicity ability in vitro, whereas knockdown of PBOV1 reduced these effects. Further analysis of PBOV1 overexpression inhibited cell cycle inhibitors, P21 and P27, and increased the phosphorylation level of Rb and cyclin D1 expression, suggesting that PBOV1 promoted cell proliferation through promoting G1/S transition.

摘要

前列腺癌(PC)是男性癌症死亡的主要原因之一,因此,寻找新的调控因子对前列腺癌治疗至关重要。前列腺和乳腺癌过表达1(PBOV1)在乳腺癌、前列腺癌和膀胱癌中过表达,因为它在前列腺癌患者血清中上调,但PBOV1在前列腺癌中的作用尚未得到研究。在本文中,我们发现PBOV1在前列腺癌细胞中确实过表达;PBOV1过表达促进细胞增殖和集落形成能力,并使细胞周期停滞在G0/G1期,且在体外具有致瘤能力,而敲低PBOV1可降低这些作用。对PBOV1过表达的进一步分析显示,它抑制细胞周期抑制剂P21和P27,并增加Rb的磷酸化水平和细胞周期蛋白D1的表达,这表明PBOV1通过促进G1/S转换来促进细胞增殖。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6289/4762445/dec15a27f749/ott-9-787Fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6289/4762445/44c77878bc2a/ott-9-787Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6289/4762445/885093efd451/ott-9-787Fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6289/4762445/9d4ecbec3588/ott-9-787Fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6289/4762445/dec15a27f749/ott-9-787Fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6289/4762445/44c77878bc2a/ott-9-787Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6289/4762445/885093efd451/ott-9-787Fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6289/4762445/9d4ecbec3588/ott-9-787Fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6289/4762445/dec15a27f749/ott-9-787Fig4.jpg

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