膀胱癌
活力测定
转染
癌症研究
小RNA
细胞生长
HMGA2型
细胞凋亡
免疫印迹
流式细胞术
癌细胞
化学
自噬
癌症
细胞
细胞培养
生物
分子生物学
医学
内科学
基因
生物化学
遗传学
作者
Shouchun Li,Minjie Pan,Xiaopeng Wu,Yu Bai,Minjun Qi,Jiasheng Chen,Li Zuo
出处
期刊:PubMed
日期:2023-07-01
卷期号:53 (4): 607-618
被引量:1
摘要
MicroRNAs have been reported to be involved in the regulation of tumor progression. This study investigated the role of miR-152-3p in bladder cancer development.A total of 67 bladder cancer cases were enrolled. miR-152-3p expression in bladder cancer tissues and cells were detected using quantitative reverse transcriptase polymerase chain reaction. Bladder cancer cells were transfected by miR-152-3p mimic and inhibitor to up-regulate and down-regulate miR-152-3p expression. After transfection, cell counting kit-8 assay, flow cytometry, Brdu staining assay, transwell experiment and wound healing assay were conducted to research the effect of miR-152-3p up-regulation/down-regulation on bladder cancer cell viability, apoptosis, proliferation, invasion and migration abilities. The expression of high-mobility group protein A2 (HMGA2) and autophagy-related proteins was researched using Western blot. The interaction between miR-152-3p and HMGA2 was explored by dual luciferase reporter gene assay.Low miR-152-3p expression in tumor tissues bladder cancer patients was associated with poor prognosis. miR-152-3p expression was abnormally down-regulated in bladder cancer cells. miR-152-3p up-regulation inhibited viability, proliferation, invasion, migration but promoted apoptosis of bladder cancer cells. miR-152-3p down-regulation showed the opposite effects. miR-152-3p up-regulation suppressed the expression of Beclin 1 and LC3II/LC3I proteins in bladder cancer cells, but miR-152-3p down-regulation increased them. HMGA2 was target of miR-152-3p, which could be directly inhibited by miR-152-3p. HMGA2 up-regulation reversed the inhibitory effect of miR-152-3p on bladder cancer cell malignant phenotype.miR-152-3p inhibited malignant phenotype of bladder cancer cell lines via suppressing HMGA2 expression.
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