论文部分内容阅读
目的:探讨微小RNA（miRNA）-4795-3p通过靶基因表皮生长因子受体（epidermal growth factor receptor，EGFR）抑制胃癌细胞增殖和侵袭。方法:本研究于2020年6月至12月分别转染阴性对照模拟物（阴性对照组）和miR-4795-3p模拟物（miR-4795-3p组）至胃癌BGC823细胞。实时定量聚合酶链反应（qRT-PCR）检验转染效率。淋巴细胞增殖检测（MTS）法和Transwell实验检测BGC823细胞的增殖情况及侵袭能力。生物信息学软件miRcode预测miR-4795-3p的靶基因，采用双荧光素酶报告基因实验验证miR-4795-3p与靶基因的结合。qRT-PCR和蛋白质免疫印迹试验（Western blot）检测靶基因的表达。采用SPSS 21.0软件分析数据，组间比较应用独立样本n t检验，n P<0.05为差异有统计学意义。n 结果:miR-4795-3p组和阴性对照组BGC823细胞中miR-4795-3p表达分别为（1.02±0.11）和（11.04±1.23），阴性对照组miR-4795-3p表达明显低于miR-4795-3p组（n t=8.14，n P<0.01）。与阴性对照组比较，miR-4795-3p组BGC823细胞吸光度值明显下降（n P<0.05），细胞侵袭数明显减少（n P<0.01）。miR-4795-3p与EGFR存在互补结合位点，miR-4795-3p可互补结合EGFR（n P<0.01）。与阴性对照组比较，miR-4795-3p组BGC823细胞中EGFR表达明显降低（n P<0.01）。n 结论:miR-4795-3p通过靶向负调控EGFR抑制胃癌BGC823细胞的增殖和侵袭能力。“,”Objective:To investigate the effect of microRNA (miR)-4795-3p on the proliferation and invasion of gastric cancer cells by regulating the expression of epidermal growth factor receptor (EGFR).Methods:The negative control mimic (a negative control group) and miR-4795-3p mimic (a miR-4795-3p group) were respectively transfected into the gastric cancer BGC823 cells from June to December 2020. Real-time polymerase chain reaction (qRT-PCR) was used to test the transfection efficiency. The MTS method and Transwell experiment were used to detect the proliferation and invasion ability of the BGC823 cells. The bioinformatics software miRcode predicted the target gene of miR-4795-3p, and the dual luciferase reporter gene experiment was used to verify the binding of miR-4795-3p to the target gene. qRT-PCR and Western blot were used to detect the target gene expression. The software SPSS 21.0 was used to analyzed the data. The independent-sample n t test was used for the comparison between the groups. If n P<0.05, there is a statistical difference.n Results:The expressions of miR-4795-3p in the BGC823 cells of the miR-4795-3p group and the negative control group were (1.02±0.11) and (11.04 ± 1.23), respectively. The expression of miR-4795-3p in the negative control group was significantly lower than that in the miR-4795-3p group (n t=8.14, n P<0.01). Compared with those in the negative control group, the absorbance of the BGC823 cells in the miR-4795-3p group was significantly decreased (n P<0.05), and the number of cell invasion was significantly reduced (n P<0.01). miR-4795-3p and EGFR had complementary binding sites, and miR-4795-3p could complementally bind to EGFR (n P<0.01). Compared with that in the negative control group, the expression of EGFR in the BGC823 cells in the miR-4795-3p group was significantly reduced (n P<0.01).n Conclusion:miR-4795-3p inhibits the proliferation and invasion of gastric cancer BGC823 cells by targeting and negatively regulating EGFR expression.