ABSTRACT
Objective:To investigate the effects of radix actinidiae chinensis extracts on the proliferation and apoptosis of breast cancer cells by regulating the vascular endothelial growth factor (VEGF)/phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway.Methods:Human breast cancer cell line MCF7 was cultured in vitro and divided into control group, low-dose group, medium dose group and high-dose group. The low-dose, medium dose and high-dose groups were added with DMEM culture medium diluted with 1, 10 and 100 μg/ml radix actinidiae chinensis extracts respectively. The control group was added with equal dose DMEM culture medium for 48 hours. The proliferation rate (detected by methyl thiazolyl tetrazolium method), apoptosis rate (detected by flow cytometry) and the protein expression of PI3K, VEGF and phosphorylation-AKT(p-AKT) in each group were compared (detected by Western blot). Results:Compared with the control group, the proliferation rate and PI3K, VEGF, p-AKT protein expression of MCF7 cells in low dose group were significantly decreased ( P<0.05), and the apoptosis rate of MCF7 cells in low dose group was significantly increased ( P<0.05); compared with low dose group, the proliferation rate and PI3K, VEGF, p-AKT protein expression of MCF7 cells in medium dose group were significantly decreased ( P<0.05), and the apoptosis rate of MCF7 cells in medium dose group was significantly increased ( P<0.05). Compared with the middle dose group, the proliferation rate of MCF7 cells and the expression of PI3K, VEGF and p-AKT protein in the high dose group were significantly decreased ( P<0.05), and the apoptosis rate of MCF7 cells in the high dose group was significantly increased ( P<0.05). Conclusions:Radix actinidiae chinensis extracts may inhibit the proliferation and promote the apoptosis of breast cancer cells by inhibiting the VEGF/PI3K/AKT signaling pathway.
ABSTRACT
Objective:To investigate the effect of microRNA-144-3p (miRNA-144-3p) on drug resistance sensitivity of thyroid cancer cells by targeting and regulating paired box gene 8 (PAX8).Methods:Human thyroid cancer cell line FTC-133 was cultured in vitro and selected to construct the cisplatin-resistant cell stains. Reverse transcription polymerase chain reaction (RT-PCR) was used to detect the relative expression of miRNA-144-3p in FTC-133 cells and cisplatin-resistant FTC-133 cells. The cisplatin-resistant FTC-133 cells were divided into group A, group B, and group C. Group A received no treatment, group B was transfected with empty plasmids, and group C was transfected with pCDNA3.1+ miRNA-144-3p plasmids. RT-PCR was used to detect the relative expression levels of miRNA-144-3p and PAX8 in each group, and methyl thiazolyl tetrazolium (MTT) method was used to detect the half inhibitory concentration (IC 50) value of cisplatin on cells in each group, proliferation rate in each group was detected by cell counting kit-8 (CCK-8) method, and apoptosis rate in each group was detected by flow cytometry. Results:The relative expression level of miRNA-144-3p in cisplatin-resistant FTC-133 cells was significantly higher than that of FTC-133 cells [(0.93±0.24) vs (0.26±0.04), P<0.05]; The IC 50 value, proliferation rate, apoptosis rate and relative expression levels of miRNA-144-3p and PAX8 in cisplatin-resistant FTC-133 cells in group B were not significantly different from those in group A ( P>0.05). The IC 50 value, proliferation rate and relative expression of miRNA-144-3p of cisplatin resistant FTC-133 cells in group C were significantly higher than those in group B ( P<0.05), and apoptosis rate and relative expression of PAX8 were significantly lower than those in group B ( P<0.05). Conclusions:Overexpression of miRNA-144-3p may increase cisplatin resistance of thyroid cancer cells by up-regulating PAX8 gene expression, thus promoting the proliferation of thyroid cancer cells and inhibiting their apoptosis.