MicroRNA-30c-2-3p represses malignant progression of gastric adenocarcinoma cells via targeting ARHGAP11A

MicroRNAs are crucial tumor regulators to tumor development and progression. MiR-30c-2-3p can suppress malignant progression of tumor cells, but no study has reported the modulatory process of miR-30c-2-3p in gastric adenocarcinoma (GA). We herein investigated role of miR-30c-2-3p in GA cells. Here, we evaluated gene level in cancer cells by qRT-PCR. CCK-8, colony formation, flow cytometry, and transwell assays revealed biological functions of miR-30c-2-3p and ARHGAP11A. Genes downstream of miR-30c-2-3p were acquired through bioinformatics analysis. Our results suggested a low level of miR-30c-2-3p in GA tissue and cells, while its high expression could repress the malignant progression and promote cell cycle arrest and apoptosis of GA cells. Besides, ARHGAP11A was downstream of miR-30c-2-3p, with up-regulated ARHGAP11A facilitating malignant progression and repressing cell cycle arrest and apoptosis of GA cells. In addition, changes in GA cell functions caused by high ARHGAP11A expression could be partially offset by enhancing miR-30c-2-3p. Thus, our observations indicated that miR-30c-2-3p was a tumor repressor that could inhibit GA progression via modulating ARHGAP11A.

微小核糖核酸（MicroRNAs）是调控肿瘤发生与进展的关键因子。miR-30c-2-3p可抑制肿瘤细胞的恶性进展，但目前尚无研究报道miR-30c-2-3p在胃腺癌（gastric adenocarcinoma, GA）中的调控机制。本研究旨在探究miR-30c-2-3p在胃腺癌细胞中的作用。本研究通过实时荧光定量聚合酶链反应（qRT-PCR）检测癌细胞中的基因表达水平；采用CCK-8法、集落形成实验、流式细胞术及Transwell实验分析miR-30c-2-3p与ARHGAP11A的生物学功能；通过生物信息学分析筛选得到miR-30c-2-3p的下游靶基因。结果显示，胃腺癌组织及细胞中miR-30c-2-3p呈低表达；高表达miR-30c-2-3p可抑制胃腺癌细胞的恶性进展，促进其细胞周期阻滞与凋亡。此外，ARHGAP11A是miR-30c-2-3p的下游靶基因，ARHGAP11A高表达可促进胃腺癌细胞的恶性进展，抑制其细胞周期阻滞与凋亡。进一步研究发现，过表达ARHGAP11A所引发的胃腺癌细胞功能改变，可通过上调miR-30c-2-3p的表达得到部分逆转。综上，本研究结果表明miR-30c-2-3p是一种肿瘤抑制因子，可通过调控ARHGAP11A的表达抑制胃腺癌的进展。