Passenger strand miRNA miR-31* regulates the phenotypes of oral cancer cells by targeting RhoA

Passenger strand miRNA miR-31* regulates the phenotypes of oral cancer cells by targeting RhoA
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DOI:
10.1016/j.oraloncology.2012.07.003
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发表时间:
2013-01-01
期刊:
影响因子:
4.8
通讯作者:
Lin, Shu-Chun
Lin, Shu-Chun
中科院分区:
医学2区
文献类型:
--
作者:
Chang, Kuo-Wei;Kao, Shou-Yen;Lin, Shu-Chun

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目的:microRNAs(MiRNAs)是通过RNA干扰负调控靶基因表达的内源性非编码小RNA。前miRNA发夹的加工产生miRNA双链,由miRNA(引导链)和miRNA*(客体链)组成。MIR-31是一种致癌的miRNA,在口腔鳞癌中表达上调。MiR-31*在物种间具有高度的保守性,在此基础上,本研究假设miR-31*是一个具有功能的miRNA。材料和方法:分析miR-31和miR-31*在口腔鳞癌组织和口腔癌细胞中的表达。结果:miR-31*在口腔鳞癌组织中表达上调,但表达不如miR-31丰富。MIR-31*抑制SAS和Fadu细胞的增殖和迁移。此外,miR-31*靶向RhoA的3‘非编码区,并能够下调RhoA的表达。已知RhoA表达下调可减少口腔鳞癌细胞的增殖和迁移。结论:miR-31*是一种参与调节RhoA的功能性miRNA,而miR-31*的活性似乎抵消了miR-31*在口腔鳞癌发生过程中的作用。(C)2012爱思唯尔有限公司,版权所有。
Objectives: MicroRNAs (miRNAs) are endogenous small non-coding RNAs that negatively regular target gene expression by RNA interference. The processing of the pre-miRNA hairpin generates a miRNA duplex, which consists of a miRNA (guide strand) and a miRNA* (passenger strand). miR-31 is an oncogenic miRNA and is up-regulated in oral squamous cell carcinoma (OSCC). miR-31* shows a high level of conservation across species and, based on this, this study hypothesized that miR-31* is a functional miRNA.Materials and Methods: The expression of miR-31 and miR-31* in OSCC tissues and oral cells were analyzed. Functional studies were performed on OSCC cells.Results: miR-31* is up-regulated in OSCC tissues, but its expression is less abundant than miR-31. miR-31* decreases the proliferation and migration of both SAS and Fadu cells. Furthermore, miR-31* targets the 3'UTR of RhoA and is able to down-regulate RhoA expression. Knockdown of RhoA expression is known to decrease the proliferation and migration of OSCC cells. However, up-regulation of both miR-31 and miR-31* by delivery of pre-mir-31 does still enhance OSCC oncogenicity.Conclusion: miR-31* is a functional miRNA involving in regulating RhoA, and the activity of miR-31*'s activity seems to counteract the functions of miR-31 during OSCC tumorigenesis. (C) 2012 Elsevier Ltd. All rights reserved.