miR-26a inhibits proliferation and motility in bladder cancer by targeting HMGA1
miR-26a inhibits proliferation and motility in bladder cancer by targeting HMGA1
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DOI：
10.1016/j.febslet.2013.06.021
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发表时间：
2013-08-02
期刊：
影响因子：
3.5
通讯作者：
Xie, Liping
中科院分区：
文献类型：
--
作者：
Lin, Yiwei;Chen, Hong;Xie, Liping
越来越清楚的是，microRNAs在肿瘤发生中起着至关重要的作用。近年来，越来越多的证据表明miR-26a在肿瘤组织中异常表达。在我们的研究中，我们观察到10例人膀胱癌组织中miR-26a的表达频繁下调。膀胱癌细胞株T24强制表达miR-26a可抑制细胞增殖，降低细胞运动能力。高迁移率族AT-Hook1(HMGA1)是一个调节细胞周期转换和细胞运动的基因，被证实是miR-26a在膀胱癌中的一个新靶点。这些结果提示miR-26a在膀胱癌分子病因学中的重要作用，并提示miR-26a在膀胱癌治疗中的潜在应用。(C)2013年欧洲生化学会联合会。爱思唯尔出版，版权所有。
It is increasingly clear that microRNAs play a crucial role in tumorigenesis. Recently, emerging evidence suggested that miR-26a is aberrantly expressed in tumor tissues. In our study, frequent down-regulation of miR-26a was observed in 10 human bladder cancer tissues. Forced expression of miR-26a in the bladder cancer cell line T24 inhibited cell proliferation and impaired cell motility. High mobility group AT-hook 1 (HMGA1), a gene that modulates cell cycle transition and cell motility, was verified as a novel target of miR-26a in bladder cancer. These findings indicate an important role for miR-26a in the molecular etiology of bladder cancer and implicate the potential application of miR-26a in bladder cancer therapy. (C) 2013 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.