Paclitaxel inhibits proliferation and invasion and promotes apoptosis of breast cancer cells by blocking activation of the PI3K/AKT signaling pathway

Background.Breast cancer has the highest incidence and mortality among all cancers in women.Paclitaxel (PTX) has a notable therapeutic effect on cancer in clinical practice. Objectives.To explore the effect and mechanism of PTX on the proliferation, apoptosis and invasiveness of breast cancer cells.Material and methods.MCF-7 cells were treated with PTX (0 μM, 0.01 μM, 0. 1 μM, 1 μM) for 48 h.Cell viability was detected using MTT assay and lactate dehydrogenase (LDH) assay; the cell proliferation rate was detected using 5-ethynyl-2'-deoxyuridine (EdU) assay to screen the most effective concentration of PTX.MCF-7 cells were then divided into 5 groups: control group, PTX group, oe-PI3K group, NC-PI3K group, and oe-PI3K+PTX group.Cell apoptosis and cell cycles were detected with flow cytometry; cell invasion was determined using a transwell assay; western blot and quantitative reverse-transcription polymerase chain reaction (qRT-PCR) were used to measure the mRNA and protein expression level of cleaved caspase-3, Bax, Bcl-2, matrix metalloproteinase 9 (MMP-9), vascular endothelial growth factor (VEGF), p-AKT (Thr308), and p-AKT (Ser473).Results.Paclitaxel inhibited cell viability and proliferation in a dose-dependent manner.In the PTX group, the apoptosis rate, the number of cells arrested in the G2/M phase and the expression levels of Cleaved caspase-3 and Bax were increased, but the number of invasive cells and the expression levels of Bcl-2, MMP-9, vascular endothelial growth factor (VEGF), p-AKT (Thr308), and p-AKT (Ser473) were decreased.However, PI3K upregulation can reverse the effects of PTX. Conclusions.Paclitaxel could inhibit MCF-7 cell proliferation and invasion, and promote MCF-7 cell apoptosis by downregulating the expression of p-AKT (Thr308) and p-AKT (Ser473) in the PI3K/AKT signaling pathway.