Department of Medical Laboratory, The First Affiliated Hospital, Zhengzhou University, Zhengzhou, Henan Province, China.
Biomed Pharmacother. 2020 Aug;128:110313. doi: 10.1016/j.biopha.2020.110313. Epub 2020 Jun 2.
Accumulating evidence has demonstrated that long non-coding RNAs (lncRNAs) function as essential regulators in the development and progression of multiple tumors. However, the molecular mechanisms of MIR31HG in regulating ESCC progression remain unknown. Here, we confirmed that MIR31HG facilitated ESCC cells proliferation in vivo. Besides, MIR31HG knockdown increases the percentage of cells at the G1 phase, along with reduced arrest in S phase and MIR31HG overexpression exhibits the opposite effects. Overexpressed MIR31HG decreases the percentage of apoptotic ESCC cells. Interestingly, MIR31HG can function as a competing endogenous RNA by sponging miR-34a. The rescue experiments demonstrated that MIR31HG function is partially reversed by inhibiting miR-34a. In addition, we found c-Met is a target gene of miR-34a and is indirectly regulated by MIR31HG. Taken together, our findings revealed that MIR31HG promotes ESCC progression by regulating miR-34a/ c-Met axis and may provide a new prospective for exploration and understanding of the biological effects of esophageal squamous cell carcinoma.
越来越多的证据表明，长非编码 RNA（lncRNA）在多种肿瘤的发生和发展中作为重要的调节因子发挥作用。然而，MIR31HG 在调节 ESCC 进展中的分子机制尚不清楚。在这里，我们证实 MIR31HG 促进 ESCC 细胞在体内的增殖。此外，MIR31HG 敲低增加了 G1 期细胞的比例，同时减少了 S 期的停滞，而过表达则表现出相反的效果。过表达的 MIR31HG 降低了 ESCC 细胞的凋亡比例。有趣的是，MIR31HG 可以作为竞争性内源性 RNA 通过海绵吸附 miR-34a 发挥作用。挽救实验表明，通过抑制 miR-34a，MIR31HG 的功能部分逆转。此外，我们发现 c-Met 是 miR-34a 的靶基因，并且受到 MIR31HG 的间接调节。综上所述，我们的研究结果表明，MIR31HG 通过调节 miR-34a/c-Met 轴促进 ESCC 的进展，为探索和理解食管鳞状细胞癌的生物学效应提供了新的视角。
