实用临床医药杂志2025，Vol.29Issue(3)：6-10,16,6.DOI:10.7619/jcmp.20243658
微小RNA-299-3p通过磷脂酰肌醇3激酶/蛋白激酶B通路调控鼻咽癌增殖、侵袭及迁移的研究
MicroRNA-299-3p regulates proliferation,invasion and migration of nasopharyngeal carcinoma through phosphatidylinositol 3-kinase/protein kinase B pathway
摘要
Abstract
Objective To investigate the role of microRNA(miR)-299-3p in regulating the pro-liferation,invasion,and migration of nasopharyngeal carcinoma cells through phosphatidylinositol 3-ki-nase(PI3 K)/protein kinase B(AKT)signaling pathway.Methods The human nasopharyngeal car-cinoma cell line CNE2 was randomly divided into three groups:control group(no expression of miR-299-3 p),over-expression group overexpression of miR-299-3p,and miR-299-3p low-expression group(low expression of miR-299-3p).CCK-8 experiment was to detect cell proliferation rate,flow cytome-try was to detect apoptosis rate,Transwell chamber was to detect invasion and migration,Western blot was to detect p-PI3K and p-AKT protein expressions,real-time fluorescence quantitative polymerase chain reaction was to detect miR-299-3p expressions.Results Compared with the control group,the over-expression group showed significant decreases in cell proliferation rate,the number of cells with invasion and migration,increase in apoptosis rate;compared with the control group,the low-expres-sion group showed significant increases in cell proliferation rate,the number of cells with invasion and migration,phosphorylated PI3K(p-PI3K)and phosphorylated AKT(p-AKT)protein expression,de-crease in apoptosis rate(P＜0.05).Conclusion Over-expression of miR-299-3p may affect the pro-liferation,invasion,and migration behaviors of nasopharyngeal carcinoma cells by inhibiting PI3K/AKT signaling pathway activity.关键词
鼻咽癌/微小RNA-299-3p/磷脂酰肌醇3激酶/蛋白激酶BKey words
nasopharyngeal carcinoma/microRNA-299-3p/phosphatidylinositol 3-kinase/pro-tein kinase B分类
医药卫生引用本文复制引用
穆热迪力·穆塔里甫,阿卜拉·艾则孜,皮力东·库亚西,张维娜,雍军..微小RNA-299-3p通过磷脂酰肌醇3激酶/蛋白激酶B通路调控鼻咽癌增殖、侵袭及迁移的研究[J].实用临床医药杂志,2025,29(3):6-10,16,6.基金项目
新疆维吾尔自治区自然科学基金项目(2021D01C320) （2021D01C320）
