Effects of miR-369-3p on the proliferation and apoptosis of bladder cancer cells by regulating the expression of VEGFC gene
10.3760/cma.j.issn.1008-1372.2018.01.023
- VernacularTitle:miR-369-3p通过调控VEGFC基因表达对膀胱癌细胞增殖及凋亡的影响
- Author:
Zhenling ZHAO
1
;
Huanjun SHAO
;
Lina HAO
;
Jun LIU
Author Information
1. 236800,安徽省亳州市人民医院泌尿外科
- Keywords:
MicroRNAs/PD;
Vascular endothelial growth factor C/DE/ME;
Urinary bladder neoplasms/DT/PA/ME;
Cell proliferation/DE;
Apoptosis/DE
- From:
Journal of Chinese Physician
2018;20(1):92-95,99
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the effect of miR-369-3p on vascular endothelial growth factor C (VEGFC) gene in bladder cancer cells EJ and 5637 and observe its effect on cell proliferation and apoptosis.Methods Bladder cancer cell lines EJ and 5637 were transfected with miR-NC (control group) or transfected with miR-369-3p (experimental group).The target gene of miR-369-3p was predicted by Targets can target gene prediction software.Fluorescence real-time quantitative polymerase chain reaction (qPCR) was used to detect the changes of VEGFC at mRNA level.The changes of VEGFC,p-Raf-1 and phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2) at the protein level were detected by Western blotting.The effect of miR-369-3p on the proliferation of bladder cancer cells was detected by cell counting kit (CCK-8) and clone formation experiment.The effect of miR-369-3p on apoptosis was detected by flow cytometry.Results After transfection with miR-369-3p,the expression of VEGFC at mRNA and protein levels was significantly decreased (P ＜ 0.05),the expression of p-Raf-1 and p-ERK1/2 protein was significantly decreased,the cell proliferation ability was significantly decreased (P ＜ 0.05),the number of clones formed was significantly decreased (P ＜ 0.05) and the apoptosis was significantly increased (P ＜ 0.01).Conclusions miR-369-3p can inhibit the proliferation and promote the apoptosis of bladder cancer cells by interfering with the expression of VEGFC gene,which may provide a new target for the biological therapy of bladder cancer.
