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MiR-572通过抑制PPP2R2C的表达来促进人卵巢癌细胞的增殖。

MiR-572 prompted cell proliferation of human ovarian cancer cells by suppressing PPP2R2C expression.

作者信息

Wu Ai-Hua, Huang Yu-ling, Zhang Lan-Zhen, Tian Geng, Liao Qiong-Zhi, Chen Shi-Ling

机构信息

Institute of Gynecology and Obstetrics, Second Affiliated Hospital of Guangzhou Medical University, Guangzhou 510260, People's Republic of China; Center for Reproductive Medicine, Department of Gynecology and Obstetrics, Nanfang Hospital, Southern Medical University, Guangzhou 510515, People's Republic of China.

Center for Reproductive Medicine, Third Affiliated Hospital of Guangzhou Medical University, Guangzhou 510150, People's Republic of China; Center for Reproductive Medicine, Department of Gynecology and Obstetrics, Nanfang Hospital, Southern Medical University, Guangzhou 510515, People's Republic of China.

出版信息

Biomed Pharmacother. 2016 Feb;77:92-7. doi: 10.1016/j.biopha.2015.12.005. Epub 2015 Dec 28.

DOI:10.1016/j.biopha.2015.12.005
PMID:26796271
Abstract

Ovarian cancer (OC) remains one of the most common types of malignant cancer, and the molecular mechanism underlying its proliferation is still largely unclear. It is reported that microRNAs acted as important regulators of cell proliferation by regulating its targeted gene. In this study, our result showed that miR-572 was markedly upregulated in OC cell lines and clinical tissues. Results of both gain-of-function and loss-of-function experiments revealed that upregulation of miR-572 expression dramatically promoted OC cell proliferation, whereas decreased miR-572 expression significantly reduced cell proliferation. Bioinformatics analysis and luciferase reporter assays further revealed PPP2R2C, a putative tumor suppressor as a potential target of miR-572. Moreover, silencing of PPP2R2C using small interfering RNA (siRNA) counteracted the proliferation arrest by miR-572-in in OC cells. In sum, our data provide that miR-572 promoted cell proliferation in OC by targeting PPP2R2C and might serve as a therapeutic target of OC.

摘要

卵巢癌(OC)仍然是最常见的恶性肿瘤类型之一,其增殖的分子机制仍不清楚。据报道,微小RNA通过调节其靶基因而成为细胞增殖的重要调节因子。在本研究中,我们的结果显示,miR-572在OC细胞系和临床组织中显著上调。功能获得和功能丧失实验的结果均显示,miR-572表达上调显著促进OC细胞增殖,而miR-572表达降低则显著降低细胞增殖。生物信息学分析和荧光素酶报告基因检测进一步揭示,假定的肿瘤抑制因子PPP2R2C是miR-572的潜在靶点。此外,使用小干扰RNA(siRNA)沉默PPP2R2C可抵消miR-572对OC细胞增殖的抑制作用。总之,我们的数据表明,miR-572通过靶向PPP2R2C促进OC细胞增殖,可能成为OC的治疗靶点。

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