miR-132 suppresses the migration and invasion of lung cancer cells by blocking USP9X-induced epithelial-mesenchymal transition.

波形蛋白 上皮-间质转换 基因敲除 癌症研究 小RNA 细胞迁移 转移 肺癌 体外 生物 细胞培养 化学 癌症 医学 病理 免疫学 基因 免疫组织化学 生物化学 遗传学
作者
Huihui Guo,Xilin Zhang,Qiuqiang Chen,Ying Bao,Chaohui Dong,Xiang Wang
出处
期刊:PubMed 卷期号:10 (1): 224-234 被引量:9
链接
标识
摘要

miR-132, a microRNA, has been reported to be down-regulated in several human cancers and is related with tumor progression; however, its function in non-small cell lung cancer (NSCLC) progression remains unclear. This study aimed to investigate the putative role of miR-132 in the metastasis of NSCLC. We determined the function of miR-132 in the migration and invasion of a NSCLC cell line in vitro using a miR-132 inhibitor and mimic. Our results showed overexpression of miR-132 significantly inhibited the migration and invasion of NSCLC cells in vitro. We then identified USP9X as a potential target of miR-132, and demonstrated miR-132 could regulate the expression of USP9X at both the mRNA and protein level. miR-132 could directly bind to the 3' untranslated region (3'-UTR) of USP9X. Inhibition of USP9X by its inhibitor WP1130 reduced the migration and invasion of NSCLC cells. Furthermore, USP9X inhibition also reversed the increased migration and invasion mediated by miR-132 inhibition. We found USP9X inhibition up-regulated expression of the epithelial-mesenchymal transition (EMT) marker E-cadherin, but down-regulated vimentin expression. A similar effect was seen with miR-132 overexpression, while the opposite effect occurred with miR-132 knockdown. USP9X inhibition reversed the miR-132 inhibitor-induced vimentin up-regulation and E-cadherin down-regulation. Taken together, these results indicate miR-132 prohibits the migration and invasion of NSCLC cells via targeting USP9X-induced EMT. Our data provides further evidence for the critical role of miR-132 and USP9X in regulating cell invasion and migration of NSCLC.

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
1秒前
2秒前
5秒前
XJ应助顺利紫山采纳,获得10
5秒前
6秒前
钟美莲发布了新的文献求助10
7秒前
9秒前
10秒前
红宝石设计局完成签到,获得积分10
12秒前
13秒前
沉默完成签到,获得积分10
18秒前
小诗发布了新的文献求助30
18秒前
20秒前
22秒前
烟花应助Hayat采纳,获得10
24秒前
难过大神完成签到,获得积分10
25秒前
cdercder应助Rjy采纳,获得10
25秒前
27秒前
27秒前
彭于晏应助dasfdufos采纳,获得10
28秒前
mo发布了新的文献求助20
28秒前
马凯完成签到,获得积分10
28秒前
28秒前
小诗完成签到,获得积分20
28秒前
Baekhyun完成签到,获得积分10
28秒前
loin发布了新的文献求助30
32秒前
刻苦鼠标发布了新的文献求助20
32秒前
Orange应助科研通管家采纳,获得10
35秒前
元谷雪应助科研通管家采纳,获得10
35秒前
35秒前
香蕉觅云应助科研通管家采纳,获得10
35秒前
科研通AI5应助科研通管家采纳,获得10
35秒前
科研通AI5应助科研通管家采纳,获得30
35秒前
科研通AI5应助科研通管家采纳,获得200
35秒前
栀晴应助科研通管家采纳,获得20
35秒前
Owen应助Zurlliant采纳,获得10
35秒前
bkagyin应助科研通管家采纳,获得10
35秒前
35秒前
大个应助凌兰采纳,获得10
38秒前
dasfdufos发布了新的文献求助10
39秒前
高分求助中
All the Birds of the World 4000
Production Logging: Theoretical and Interpretive Elements 3000
Les Mantodea de Guyane Insecta, Polyneoptera 2000
Am Rande der Geschichte : mein Leben in China / Ruth Weiss 1500
CENTRAL BOOKS: A BRIEF HISTORY 1939 TO 1999 by Dave Cope 1000
Machine Learning Methods in Geoscience 1000
Resilience of a Nation: A History of the Military in Rwanda 888
热门求助领域 (近24小时)
化学 材料科学 医学 生物 工程类 有机化学 物理 生物化学 纳米技术 计算机科学 化学工程 内科学 复合材料 物理化学 电极 遗传学 量子力学 基因 冶金 催化作用
热门帖子
关注 科研通微信公众号,转发送积分 3738291
求助须知:如何正确求助?哪些是违规求助? 3281789
关于积分的说明 10026606
捐赠科研通 2998667
什么是DOI,文献DOI怎么找? 1645317
邀请新用户注册赠送积分活动 782748
科研通“疑难数据库(出版商)”最低求助积分说明 749901