沉默 FGF4 表达对乳腺癌细胞增殖和凋亡的影响及其机制.

Objective To investigate the effect of silencing fibroblast growth factor 4( FGF4) expression on proliferation and apoptosis of breast cancer cells and its mechanism. Methods The human breast cancer cells MCF-7( MCF-7 cells) of the second generations were randomly divided into the siRNA interference FGF4 silencing group, negative control group, and blank control group. The siRNA and negative control sequences were transfected according to the liposome LipofectamineTM2000 transfection reagent, and the blank control was not transfected. The cells of the three groups transfected for 48 h were collected, and the proliferation inhibition rate of the cells at 24, 48, and 72 h after the culture was detected by MTT assay. Flow cytometry was used to discover the early apoptosis rate of cells at 48 h. Western blotting was applied to explore the expression of cyclin D1 and caspase-3 of cells at 48 h after transfection. Methods After 24, 48, and 72 h of cultivation in each group, the cell proliferation inhibition rate of the FGF4 silencing group was significantly higher than that of the negative control and the blank control group( P < 0. 05). However, there was no statistical significance between the blank control and the negative control groups( P > 0. 05). The early apoptotic rate of the FGF4 silencing group was outstandingly higher than that of the other two groups( P < 0. 05). And no statistically significant difference was found between the blank control and the negative control group( P > 0. 05). The relative expression of cyclin D1 protein in the FGF4 silencing group was obviously lower than that of the negative control and blank control groups( P < 0. 05), and the relative expression of caspase-3 protein increased remarkably as compared with that of the other groups, but no statistical difference was found between the negative control group and the blank control group( P > 0. 05). Conclusion Silencing FGF4 expression can inhibit breast cancer cell proliferation and promote its apoptosis, and its mechanism may be related to the inhibition of cyclin D1 and promotion of caspase-3 protein expression. [ABSTRACT FROM AUTHOR]