腺病毒介导IL-24基因诱导人脑胶质瘤U87MG细胞的凋亡

Adenovirus-mediated IL-24 gene induces apoptosis of human glioma U87MG cells

目的:研究腺病毒介导IL-24基因表达载体(Ad-IL-24)对人脑胶质瘤U87MG细胞的抑制作用,初步探讨其作用机制。方法:将本科室构建的Ad-IL-24感染U87MG细胞,RT-PCR法检测IL-24基因的表达,MTT法和流式细胞术检测U87MG细胞的生长和凋亡,激光共聚焦显微镜观察U87MG细胞凋亡的形态学变化,RT-PCR法检测Bax、Bcl-2基因mRNA的表达,Western blotting检测caspase-3的活化。结果:Ad-IL-24感染U87MG细胞后,IL-24在U87MG细胞中有明显表达,并抑制U87MG细胞生长、诱导其凋亡、出现典型的凋亡细胞核形态学改变。Ad-IL-24可上调U87MG细胞中Bax基因、下调Bcl-2基因的表达,并诱导caspase-3蛋白的活化。结论:Ad-IL-24可诱导U87MG细胞凋亡,其机制可能与上调Bax基因、下调Bcl-2基因表达,并活化caspase-3有关。

Objective： To investigate the inhibitory effect of adenovirus-mediated IL-24（Ad-IL-24） on human glioma U87MG cells and to explore the underlying molecule mechanism.Methods： U87MG cells were infected with Ad-IL-24 constructed in our department,and IL-24 gene expression in U87MG cells was detected by RT-PCR.The growth and apoptosis of U87MG cells were examined by MTT and flow cytometry;the morphological change of U87MG cells was observed by laser scanning confocal microscopy;the Bax and Bcl-2 mRNA expressions were analyzed by RT-PCR;and the activation of caspase-3 was examined by Western blotting analysis.Results： The IL-24 gene was expressed in Ad-IL-24-infected U87MG cells.Ad-IL-24-infection inhibited the growth and induced apoptosis of U87MG cells,which showed typical morphological changes of apoptotic nuclei.Moreover,Ad-IL-24 increased Bax and decreased Bcl-2 mRNA expression,and induced caspase-3 activation in U87MG cells.Conclusion： Ad-IL-24 can induce apoptosis of U87MG cells,probably through up-regulating Bax expression,down-regulating Bcl-2 expression,and inducing caspase-3 activation.