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COPS3 的过表达通过调节磷酸化 AKT(Thr308)、细胞周期蛋白 D1 和半胱氨酸天冬氨酸蛋白酶 3 促进肾透明细胞癌的进展。

Overexpression of COPS3 promotes clear cell renal cell carcinoma progression via regulation of Phospho-AKT(Thr308), Cyclin D1 and Caspase-3.

机构信息

The Department of Urology, Peking University People's Hospital, Beijing, China.

出版信息

Exp Cell Res. 2018 Apr 15;365(2):163-170. doi: 10.1016/j.yexcr.2018.02.025. Epub 2018 Feb 23.

Abstract

The third subunit of the COP9 signalosome (COPS3) is associated with cell proliferation and tumorigenesis process in cancer. The present study showed that the expression level of COPS3 was upregulated in malignant cell lines and COPS3 overexpression was related with clinical stage, T stage, historical grade. Kaplan-Meier survival curves showed that COPS3 may function as a prognostic factor for overall survival. CCK-8 and colony formation assays revealed that knockdown of COPS3 in ACHN and 786-O significantly impacted proliferation in vitro. In addition, flow cytometry showed that inhibition of COPS3 induced G0/G1 arrest and promoted apoptosis. COPS3 may promote kidney cancer progression by altering Phospho-AKT(Thr308), Cyclin D1 and Caspase-3 expression. Collectively, Our findings suggest that COPS3 may be a new potential target of ccRCC.

摘要

COP9 信号osome 的第三个亚基(COPS3)与癌症中的细胞增殖和肿瘤发生过程有关。本研究表明,COPS3 的表达水平在恶性细胞系中上调,并且 COPS3 的过表达与临床分期、T 分期、历史分级有关。Kaplan-Meier 生存曲线表明 COPS3 可能是总生存的预后因素。CCK-8 和集落形成测定显示,在 ACHN 和 786-O 中敲低 COPS3 显著影响体外增殖。此外,流式细胞术显示抑制 COPS3 诱导 G0/G1 期阻滞并促进细胞凋亡。COPS3 可能通过改变磷酸化-AKT(Thr308)、细胞周期蛋白 D1 和 Caspase-3 的表达来促进肾癌的进展。综上所述,我们的研究结果表明,COPS3 可能是 ccRCC 的一个新的潜在靶点。

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