Department of Life Science and Engineering, Jining University, Qufu, Shandong, China.
Department of Nursing, Affiliated Hospital of Jining Medical University, Jining, Shandong, China.
Aging (Albany NY). 2020 Jun 18;12(12):12107-12118. doi: 10.18632/aging.103379.
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, 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.
miRNA-126(miR-126)已被证明参与各种恶性肿瘤以及其他生物学过程。然而,目前其在食管鳞状细胞癌(ESCC)中的作用尚不清楚。本研究集中于阐明 miR-126 对 ESCC 细胞存活和死亡(凋亡和自噬)的影响机制。研究发现 miR-126 在 ESCC 细胞和组织中表达增强。下调 miR-126 抑制细胞存活,TUNEL 染色表明 miR-126 抑制促进 ESCC 细胞死亡。此外,抑制 miR-126 后,LC3B 和 p62 两种自噬信号蛋白的产生减少。双荧光素酶报告基因检测表明,STAT3 3'-UTR 是 miR-126 的直接靶标。此外,敲低 STAT3 可挽救 miR-126 抑制对 ESCC 细胞自噬和凋亡的影响。本研究结果可能为 ESCC 发生的分子和生物学机制提供一些见解,并有助于开发 ESCC 的新型治疗方法。