Transplant Medical Center, The Second Affiliated Hospital of Guangxi Medical University , Nanning, Guangxi 530007, China.
Department of Operation Room, The Second Nanning People's Hospital, Nanning, Guangxi 530031, China.
Cell Mol Biol (Noisy-le-grand). 2024 Apr 28;70(4):191-195. doi: 10.14715/cmb/2024.70.4.30.
This study aimed to explore the influence of circFOXM1/miR-218-5p molecular axis in the proliferation, apoptosis and migration of glioma cells. The levels of circFOXM1 and miR-218-5p in glioma and adjacent tissues were tested by qRT-PCR. Cultured human glioma U251 cells were randomly split into groups: si-NC, si-circFOXM1, miR-NC, miR-218-5p, si-circFOXM1+anti-miR-NC, si-circFOXM1+anti-miR-218-5p. MTT method, plate clone formation, flow cytometry and Transwell experiments were utilized for detecting the proliferation, clone formation, apoptosis and migration of glioma cells. Dual-luciferase reporter experiment authenticated the targeted relation of circFOXM1 and miR-218-5p. Western blot tested the levels of E-cadherin and N-cadherin. CircFOXM1 was upregulated while miR-218-5p was low expressed in glioma tissues versus normal tissues. After circFOXM1 silence or miR-218-5p overexpression, miR-218-5p level was increased, and cell apoptosis rate and E-cadherin expression were enhancive, whereas cell proliferation, cell clone formation and migration abilities, and N-cadherin level were reduced. CircFOXM1 could affect miR-218-5 level by negative regulation. Furthermore, miR-218-5p silence could reverse the stimulative influence of si-circFOXM1 on apoptosis rate, and E-cadherin level, and the repressive effect on cell viability, cell number of colony formation and migration, and N-cadherin expression. Inhibition of circFOXM1 expression could block the proliferation, clone formation, and migration and induce apoptosis of glioma cells by upregulating miR-218-5p.
本研究旨在探讨 circFOXM1/miR-218-5p 分子轴对胶质瘤细胞增殖、凋亡和迁移的影响。采用 qRT-PCR 检测胶质瘤及相邻组织中 circFOXM1 和 miR-218-5p 的水平。将培养的人胶质瘤 U251 细胞随机分为 si-NC 组、si-circFOXM1 组、miR-NC 组、miR-218-5p 组、si-circFOXM1+anti-miR-NC 组、si-circFOXM1+anti-miR-218-5p 组。采用 MTT 法、平板克隆形成实验、流式细胞术和 Transwell 实验检测胶质瘤细胞的增殖、克隆形成、凋亡和迁移。双荧光素酶报告实验验证 circFOXM1 和 miR-218-5p 的靶向关系。Western blot 检测 E-钙黏蛋白和 N-钙黏蛋白的水平。与正常组织相比,胶质瘤组织中 circFOXM1 上调,miR-218-5p 低表达。沉默 circFOXM1 或过表达 miR-218-5p 后,miR-218-5p 水平升高,细胞凋亡率和 E-钙黏蛋白表达增强,而细胞增殖、细胞克隆形成和迁移能力以及 N-钙黏蛋白水平降低。circFOXM1 可以通过负调控影响 miR-218-5 的水平。此外,沉默 miR-218-5p 可以逆转 si-circFOXM1 对凋亡率和 E-钙黏蛋白水平的促进作用,以及对细胞活力、集落形成和迁移细胞数量和 N-钙黏蛋白表达的抑制作用。抑制 circFOXM1 表达可通过上调 miR-218-5p 抑制胶质瘤细胞的增殖、克隆形成和迁移,并诱导细胞凋亡。