过表达TNFAIP1促进替莫唑胺对人脑胶质瘤细胞U251迁移和侵袭的抑制作用  

Overexpression of TNFAIP1 Promote the Inhibitory Effect ofTemozolomide on Migration and Invasion of Glioma Cells U251

作　　者：许斐钰 陈果 龙胜文 魏晨曦 XU Feiyu;CHEN Guo;LONG Shengwen;WEI Chenxi(College of Life Sciences,Hunan Normal University,Changsha 410081,China)

机构地区：[1]湖南师范大学生命科学学院,长沙410081

出　　处：《激光生物学报》2021年第2期178-184,共7页Acta Laser Biology Sinica

基　　金：国家自然科学基金面上项目(81972642);国家自然科学基金青年科学基金项目(21806036)。

摘　　要：为了深入研究人脑胶质瘤治疗时耐药的发生机制,并寻求潜在的治疗手段,以人脑胶质瘤细胞U251为研究对象,研究肿瘤坏死因子α诱导蛋白1(TNFAIP1)对其迁移和侵袭的影响。半定量PCR和蛋白质免疫印迹(Western blot)试验发现,替莫唑胺(TMZ)会上调U251细胞内TNFAIP1的表达。在U251细胞中过表达TNFAIP1后,发现上调TNFAIP1的表达能促进TMZ对U251细胞迁移及侵袭的抑制作用,并且这一作用是通过抑制上皮-间充质转化(EMT)信号通路来实现的。这一发现有助于为人脑胶质瘤的临床治疗提供新的理论依据,为其治疗方法提供新的策略。In order to further study the mechanism of chemotherapy resistance in human gliomas and explore potential therapeutic methods,we investigated the effects of tumor necrosis factorα-induced protein 1(TNFAIP1)on migration and invasion.Reverse transcription PCR and Western blot assays showed that temozolomide increased the expression of TNFAIP1.We overexpressed TNFAIP1 in U251 cells,then we found it could promote the inhibition of temozolomide(TMZ)on migration and invasion of U251 cells,and this effect was achieved by inhibiting epithelial-to-mesenchymal transition(EMT)signaling pathway.This finding is helpful to provide a new theoretical basis for clinical treatment of human glioma and provide a new strategy for its treatment.

关 键 词：人脑胶质瘤 TNFAIP1 TMZ 细胞侵袭 EMT 

分 类 号：Q786[生物学—分子生物学]