An inhibitory effect of miR-22 on cell migration and invasion in ovarian cancer

被引:77
作者
Li, Jun
Liang, Shanhui
Yu, Hailin
Zhang, Jin [2 ]
Ma, Duan [2 ]
Lu, Xin [1 ]
机构
[1] Fudan Univ, Obstet & Gynecol Hosp, Dept Gynecol, Shanghai 200433, Peoples R China
[2] Fudan Univ, Inst Biomed Sci, Shanghai 200433, Peoples R China
关键词
Ovarian neoplasm; miR-22; Invasion; Metastasis; EXPRESSION; MICRORNAS; CONTRIBUTES; SUPPRESSOR;
D O I
10.1016/j.ygyno.2010.08.034
中图分类号
R73 [肿瘤学];
学科分类号
100214 [肿瘤学];
摘要
Objectives. Aberrant expression of microRNAs (miRNAs) has been implicated in ovarian carcinoma. However, roles of miRNAs in ovarian caner metastasis have not been comprehensively addressed. This work is aimed to identify selected miRNAs involved in ovarian cancer metastasis. Methods. We examined the distinct miRNA expression profiles between paired high-metastatic human serous ovarian cancer cell SKOV-3ip and low-metastatic human serous ovarian cell SKOV-3 using miRNA microarray. Subsequently, a validation with Real-time RT-PCR was performed for miR-22 expression level, and a functional study was carried out for miR-22. Results. Through a screen with microarray, we found there were a variety of miRNAs differentially expressed between paired high and low metastatic serous ovarian cancer cells. Particularly, miR-22 was identified as a potential metastasis-inhibitor in ovarian cancer. There was a negative correlation between miR-22 expression and the metastatic potential in ovarian cancer cells. Furthermore, both gain-of-function and loss-of-function studies displayed an inhibitory effect of miR-22 on cell migration and invasion in vitro without significantly affecting cell viability and apoptosis. Subsequent bioinformatics analysis revealed that miR-22 might regulate multiple pro-metastatic genes, which could provide an explanation to the inhibitory effects of miR-22 on cell migration and invasion. Conclusions. Taken together, our findings suggested that miR-22 might be involved in inhibiting ovarian cancer metastasis. (C) 2010 Elsevier Inc. All rights reserved.
引用
收藏
页码:543 / 548
页数:6
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