Effect of miR-3619-5p on proliferation and apoptosis of breast cancer cell MCF-7 and T47D and its molecular mechanism
10.13315/j.cnki.cjcep.2017.11.007
- VernacularTitle:miR-3619-5p对乳腺癌细胞MCF-7和T47D增殖、凋亡的影响及分子机制
- Author:
Zhi-Min REN
1
;
Ya-Li GU
;
Xin-Min LI
;
Yao ZHANG
Author Information
1. 河南大学附属郑州市妇幼保健院病理科 450012
- Keywords:
breast neoplasm;
miR-3619-5p;
p21;
cell cycle;
apoptosis
- From:
Chinese Journal of Clinical and Experimental Pathology
2017;33(11):1209-1213
- CountryChina
- Language:Chinese
-
Abstract:
Purpose To investigate the effect of miR-3619-5p transfection on the proliferation and apoptosis of breast cancer cell lines MCF-7 and T47D and its molecular mechanism.Methods According to the different treatment,breast cancer cells were divided into two groups:control group (transfected with dsControl) and experimental group (transfected with miR3619-5p).5-ethynyl-2'-deoxyuridine (EdU) proliferation assay and colony forming assay were used to detect the proliferation ability of breast cancer cells.Flow cytometry (FCM) was conducted to analyze the cell cycle distribution and cell apoptosis.The expression of p21,CDK6 and Cyclin D1 mRNA were tested by qRT-PCR.The expression of p21,CDK6 and Cyclin D1 protein were detected by Western blot.Results The proliferation ability of breast cancer cells transfected with miR-3619-5p was significantly lower than that of control (P ＜ 0.05).Compared with the control group,the percentage of cells in the G0/G1 phase was significantly higher than that in the dsControl group,and the proportion of the cells in the S phase and G2/M phase was significantly decreased after miR-3619-Sp transfection,the cell apoptosis rate increased significantly.The expression of p21 mRNA was significantly up-regulated (P ＜ 0.01 both in the two cell lines transfected with miR-3619-5p compared with the control group,while the expression of CDK6 and Cyclin D1 mRNA was down-regulated (P ＜0.01).Western blot results were consistent with qRT-PCR results.Conclusion miR3619-5p can significantly inhibit the proliferation of breast cancer cells and promote cell apoptosis.Its molecular mechanism may be the activation of tumor suppressor gene p21 expression in breast cancer cells.
