| Objective To study the role of miR-574-3p in the sensitivity of triple-negative breast cancer cells to paclitaxel (PTX). Methods Stable transfection cell lines were constructed and divided into the non-transfection group, miR-negative control (miR-NC) group and miR-574-3p overexpression group according to cell transfection conditions. Cell proliferation under different concentrations of paclitaxel was detected by cell counting kit 8 (CCK-8) (subgroup blank group and control group were set up in the non-transfected group), and the mRNA expression level of pigmentation box homology 2(CBX2) was detected by real-time fluorescence quantitative polymerase chain reaction (PCR). The expression level of CBX2 protein was detected by Western blotting, cell invasion and migration were evaluated by Transwell assay, and cell migration was assessed by scratch assay. Results The results of CCK-8 assay showed that paclitaxel inhibited the growth of triple negative breast cancer MDA-MB-231 cells in a dose-dependent manner in all groups, but under different concentrations of paclitaxel (0.05, 0.15, 0.45, 1.35, 4.05, 8.10 μmol/L), the growth inhibition effect of miR-574-3p overexpression group was higher than that of control group and miR-NC group (P＜0.05). Real-time fluorescence quantitative PCR results showed that under the treatment of 2.10 μmol/L paclitaxel, the mRNA expression level of CBX2 in the miR-574-3p overexpression group was lower than that in the untransfected group and miR-NC group (P＜0.05). Western blot results showed that under the treatment of 2.10 μmol/L paclitaxel, the expression level of CBX2 protein in the miR-574-3p overexpression group was lower than that in the untransfected group and miR-NC group (P＜0.05). The results of Transwell detection and scratch test showed that under the treatment of 2.10 μmol/L paclitaxel, the cell invasion and migration ability of the miR-574-3p overexpression group was lower than that of the untransfected group and miR-NC group (P＜0.05). Conclusions MiR-574-3p may enhance the sensitivity of triple-negative breast cancer cells to paclitaxel by down-regulating CBX2, and inhibit the invasion and migration ability of triple-negative breast cancer cells. |
