MiR-126 promotes esophageal squamous cell carcinoma via inhibition of apoptosis and autophagy

被引:20
|
作者
Li, Mingli [1 ]
Meng, Xiangli [2 ]
Li, Mingxuan [2 ]
机构
[1] Jining Univ, Dept Life Sci & Engn, Qufu, Shandong, Peoples R China
[2] Jining Med Univ, Dept Nursing, Affiliated Hosp, Jining, Shandong, Peoples R China
来源
AGING-US | 2020年 / 12卷 / 12期
基金
中国博士后科学基金;
关键词
miR-126; esophageal squamous cell carcinoma; STAT3; apoptosis; autophagy; CANCER CELLS; PROLIFERATION; ACTIVATION; INVASION; OVEREXPRESSION; EXPRESSION; MIGRATION; MICRORNA; SURVIVAL; STAT3;
D O I
10.18632/aging.103379
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
MiRNA-126 (miR-126) has been shown to be involved in various malignancies as well as other biological processes. However, currently, its role in esophageal squamous cell carcinoma (ESCC) is not well understood. The present study is focused on the mechanisms that underlie the effect of miR-126 on cell survival and death (apoptosis and autophagy) in ESCC cells. MiR-126 expression was found to be enhanced in ESCC cells and tissues. Downregulation of miR-126 suppressed cell survival, and TUNEL staining indicated that miR-126 inhibition promoted ESCC cell death. In addition, the production of LC3B and p62 proteins, two autophagy signals, was reduced following miR-126 inhibition. A dual luciferase reporter assay demonstrated that the STAT3 3 ? -UTR is a direct target of miR-126. Furthermore, STAT3 knock -down rescued the effects on autophagy and apoptosis caused by miR-126 inhibition in ESCC cells. The results of this study may provide some insight into the molecular and biological mechanisms underlying ESCC generation and contribute to the development of novel therapeutic approaches for ESCC.
引用
收藏
页码:12107 / 12118
页数:12
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