miR-383-5p靶向ZEB2抑制食管癌细胞侵袭及间质转化

miR-383-5p targeted ZEB2 to inhibit invasion and mesenchymal transformation of esophageal cancer cells

目的:探讨miR-383-5p靶向调节ZEB2对食管癌细胞增殖、侵袭及间质转化的影响。方法:RT-PCR验证miR-383-5p过表达效率;荧光素酶报告基因实验验证ZEB2和miR-383-5p的靶向关系;Western blot检测ZEB2蛋白、内皮生长因子(VEGF)、上皮-间质转化相关蛋白(E-cad、N-Cad)表达;CCK8法检测细胞增殖;Transwell检测细胞侵袭。结果:初步确定miR-383-5p可靶向作用于ZEB2的3’UTR,且可在转录后水平负调控ZEB2表达。与ZEB2组相比,miR-383-5p/ZEB2联合转染组Eca-109细胞增殖率、侵袭细胞数及相关蛋白表达均明显降低,E-cad表达减少、N-cad表达增多,明显抑制肿瘤上皮细胞间质转化。结论:miR-383-5p可靶向下调ZEB2,进而抑制食管癌细胞Eca-109增殖、侵袭及上皮-间质转化,缓解食管癌发生发展。

Objective:To investigate effects of miR-383-5p targeting regulation of ZEB2 on proliferation,invasion and mesenchymal transformation of esophageal cancer cells.Methods:Overexpression efficiency of miR-383-5p was verified by RT-PCR.Luciferase reporter gene assay was used to detect target relationship between ZEB2 and miR-383-5p;expressions of ZEB2 protein,endothelial growth factor(VEGF),proteins associated with epithelial-mesoplasmic transformation(E-cad,N-cad)were detected by Western blot.Cell proliferation was detected by CCK8 method.Cell invasion was detected by Transwell.Results:It was preliminarily confirmed that miR-383-5p could target 3’UTR of ZEB2,and could negatively regulate expression of ZEB2 at post-transcriptional level.Compared with ZEB2 group,proliferation rate,number of invaded cells and related protein expression of Eca-109 cells in combined transfection group with miR-383-5p/ZEB2 were significantly decreased,while expression of E-cad decreased and expression of N-cad increased,which significantly inhibited the epithelial mesoplasmal transformation of tumor cells.Conclusion:miR-383-5p can downregulate ZEB2,inhibit proliferation,invasion and epithelial-mesenchymal transformation of esophageal cancer cell Eca-109,and alleviate occurrence and development of esophageal cancer.