lncRNA MALAT1靶向miR-150对口腔鳞癌细胞增殖和凋亡的影响及分子机制

Effect and molecular mechanism of lncRNA MALAT1 on proliferation and apoptosis of oral squamous carcinoma cells by targeting miR-150

目的:研究MALAT1对口腔鳞癌细胞SCC-25增殖、凋亡的影响,并探讨其机制。方法:运用qRT-PCR检测人口腔鳞癌细胞SCC-25、人永生化口腔上皮细胞HIOEC中MALAT1和miR-150的mRNA表达;将si-con组(转染si-con)、si-MALAT1组(转染si-MALAT1)、miR-150组(转染miR-150 mimics)、miR-con组(转染miR-con)、si-MALAT1+anti-miR-con组(si-MALAT1和anti-miR-con共转染)、si-MALAT1+anti-miR-150组(si-MALAT1和anti-miR-150共转染),均以脂质体法转染至SCC-25细胞;MTT法检测各组细胞的增殖;流式细胞术检测各组细胞的凋亡;双荧光素酶报告基因检测实验检测各组细胞的荧光活性。结果:与人永生化口腔上皮HIOEC细胞(Normal组)相比,口腔鳞癌SCC-25细胞(Tumor组)中MALAT1表达显著上调,miR-150显著下调(P<0.05);敲减MALAT1、过表达miR-150均可抑制SCC-25细胞增殖,促进凋亡;MALAT1靶向miR-150。抑制miR-150逆转了敲减MALAT1对口腔鳞癌细胞的增殖抑制和凋亡促进作用。结论:MALAT1可促进口腔鳞癌细胞增殖并抑制凋亡,其机制可能与靶向miR-150有关,可为口腔鳞癌的治疗提供新靶点。

Objective:To study the effect of MALAT1 on proliferation and apoptosis of oral squamous cell carcinoma cell line SCC-25,and to explore its mechanism.Methods:qRT-PCR was used to detect mRNA expression of MALAT1 and miR-150 in human oral squamous cell carcinoma cell line SCC-25 and human immortalized oral epithelial cell HIOEC.si-con group(transfected si-con),si-MALAT1 group(transfected si-MALAT1),miR-150 group(transfected miR-150 mimics),miR-con group(transfected miR-con),si-MALAT1+anti-miR-con group(co-transfected si-MALAT1 and anti-miR-con),si-MALAT1+anti-miR-150 group(co-transfected si-MALAT1 and anti-miR-150),all transfected into SCC-25 cells by liposome method.MTT assay was used to detect cell proliferation of each group.Flow cytometry was used to detect apoptosis in each group.Dual luciferase reporter assay was used to detect the fluorescence activity of each group.Results:Compared with human immortalized oral epithelial HIOEC cells(Normal group),MALAT1 was significantly up-regulated,miR-150 was significantly down-regulated in oral squamous cell carcinoma SCC-25 cells(Tumor group)(P<0.05).Knockdown of MALAT1 and overexpression of miR-150 can inhibit the proliferation and promote apoptosis of SCC-25 cells.MALAT1 targeted miR-150.Inhibition of miR-150 reversed the proliferation inhibition and apoptosis-promoting effect of MALAT1 on oral squamous cell carcinoma.Conclusion:MALAT1 can promote the proliferation and inhibit apoptosis of oral squamous carcinoma cells.The mechanism may be related to targeting miR-150,which will provide a new target for the treatment of oral squamous cell carcinoma.