MiR-372-3p inhibits the growth and metastasis of osteosarcoma cells by targeting FXYD6.

作者
Xu Sy,Xu Pf,Gao Tt
出处
期刊:PubMed [National Institutes of Health]
卷期号:22 (1): 62-69 被引量:24
标识
DOI:10.26355/eurrev_201801_14101
摘要

OBJECTIVE: Growing evidence has suggested that dysregulation of miR-372-3p may contribute to tumor development and progression in various tumors. However, the function of miR-372-3p in osteosarcoma has not been investigated. In the present study, we aimed to study the effects of miR-372-3p on osteosarcoma cell proliferation and metastasis and its regulation on FXYD6. MATERIALS AND METHODS: The expression levels of miR-372-3p and FXYD6 mRNA were quantified by RT-PCR in human osteosarcoma cell lines and tissues. The effects of miR-372-3p up-regulation on osteosarcoma cell proliferation and metastasis were assessed by MTT, wound healing assay and transwell assay. Finally, the potential regulatory effect of miR-372-3p on FXYD6 expression was confirmed. RESULTS: Our data showed that miR-372-3p was downregulated in osteosarcoma tissues compared with matched normal tissues, and the expression level of miR-372-3p was significantly lower in osteosarcoma cell lines in comparison with the normal human osteoblastic cell line. Transfection with the miR-372-3p mimic enhanced the osteosarcoma proliferation and metastasis. In vivo assay indicated that forced expression of miR-372-3p significantly suppressed tumor growth. Then, Bioinformatics prediction and experimental validation results confirmed that the function of miR-372-3p was achieved by targeting FXYD6 expression. CONCLUSIONS: Our findings revealed that miR-372-3p served as a tumor suppressor gene by targeting FXYD6 in osteosarcoma. Thus, miR-372-3 might be a potential therapeutic method for osteosarcoma.

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
平淡香岚发布了新的文献求助10
1秒前
dg_fisher发布了新的文献求助100
1秒前
dg_fisher发布了新的文献求助10
1秒前
Serein完成签到,获得积分10
2秒前
xtx发布了新的文献求助10
2秒前
beryl完成签到 ,获得积分10
3秒前
yoyo发布了新的文献求助10
3秒前
cody发布了新的文献求助30
4秒前
5秒前
dg_fisher发布了新的文献求助10
5秒前
dg_fisher发布了新的文献求助10
5秒前
dg_fisher发布了新的文献求助10
5秒前
乐空思应助clearlove采纳,获得20
5秒前
朴素凝冬完成签到 ,获得积分10
5秒前
布隆的保龄球完成签到,获得积分10
6秒前
6秒前
6秒前
7秒前
打打应助Serein采纳,获得10
7秒前
8秒前
dg_fisher发布了新的文献求助10
8秒前
dg_fisher发布了新的文献求助10
8秒前
8秒前
清脆的冰枫完成签到 ,获得积分10
8秒前
CipherSage应助友好的天奇采纳,获得10
8秒前
dg_fisher发布了新的文献求助10
8秒前
dg_fisher发布了新的文献求助10
8秒前
强强强强完成签到,获得积分10
9秒前
9秒前
11秒前
ZCM发布了新的文献求助10
11秒前
dg_fisher发布了新的文献求助20
11秒前
dg_fisher发布了新的文献求助10
11秒前
dg_fisher发布了新的文献求助30
12秒前
14秒前
14秒前
14秒前
dg_fisher发布了新的文献求助200
15秒前
bkagyin应助悦耳的易梦采纳,获得10
15秒前
dg_fisher发布了新的文献求助30
15秒前
高分求助中
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
Römisch-Germanische Forschungen 1000
APA handbook of comparative psychology: Basic concepts, methods, neural substrate, and behavior 1000
China Pluperfect I: Epistemology of Past and Outside in Chinese Art 520
Matrix Methods in Data Mining and Pattern Recognition Second Edition 510
The fast track to determining transfer functions of linear circuits: The student guide 500
The Analytical and Numerical Solution of Electric and Magnetic Fields 500
热门求助领域 (近24小时)
化学 材料科学 医学 生物 纳米技术 工程类 有机化学 化学工程 生物化学 计算机科学 内科学 物理 复合材料 催化作用 细胞生物学 无机化学 光电子学 物理化学 电极 基因
热门帖子
关注 科研通微信公众号,转发送积分 7609957
求助须知:如何正确求助?哪些是违规求助? 9185674
关于积分的说明 19677472
捐赠科研通 7183605
什么是DOI,文献DOI怎么找? 3270335
关于科研通互助平台的介绍 2434013
邀请新用户注册赠送积分活动 2264954