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miR-130a的下调通过激活胶质瘤中的HMGB2促进细胞生长和上皮-间质转化。

Downregulation of miR-130a promotes cell growth and epithelial to mesenchymal transition by activating HMGB2 in glioma.

作者信息

Tang Chunhai, Yang Zhenxiu, Chen Dongliang, Xie Qinghai, Peng Tao, Wu Jingzhan, Qi Songtao

机构信息

Department of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou City, Guangdong Province, China; Department of neurosurgery, Second Affiliated Hospital,Guangxi Medical University, Nanning City,Guangxi Province, China.

Internal Medicine-Oncology, Tenth Affiliated Hospital, Guangxi Medical University, Qinzhou City, Guangxi Province, China.

出版信息

Int J Biochem Cell Biol. 2017 Dec;93:25-31. doi: 10.1016/j.biocel.2017.08.010. Epub 2017 Aug 26.

DOI:10.1016/j.biocel.2017.08.010
PMID:28851665
Abstract

Aberrant expression of miR-130a is usually found in cancer studies; however, the role of miR-130a has seldom been reported in glioma. We explored miR-130a's function and the underlying mechanism in glioma. It was found that miR-130a expression was significantly down-regulated in glioma tissues and cell lines. Overexpression of miR-130a decreased glioma cell growth and invasion both in vitro and in vivo. We identified the oncogene HMGB2 as a downstream target of miR-130a by using luciferase and western blot assays. Knockdown of HMGB2 mimicked the effect of miR-130a in glioma cells. Taken together, our study demonstrate that miR-130a may function as a tumor suppressor in glioma and suggest that miR-130a is a potential therapeutic target for glioma patients.

摘要

在癌症研究中,通常会发现miR-130a的异常表达;然而,miR-130a在胶质瘤中的作用鲜有报道。我们探究了miR-130a在胶质瘤中的功能及其潜在机制。研究发现,miR-130a在胶质瘤组织和细胞系中表达显著下调。过表达miR-130a在体外和体内均可降低胶质瘤细胞的生长和侵袭能力。通过荧光素酶和蛋白质免疫印迹分析,我们确定癌基因HMGB2是miR-130a的下游靶点。敲低HMGB2可模拟miR-130a对胶质瘤细胞的作用。综上所述,我们的研究表明miR-130a在胶质瘤中可能发挥肿瘤抑制作用,并提示miR-130a是胶质瘤患者潜在的治疗靶点。

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