Effects of Paclitaxel on proliferation and migration of breast cancer MCF-7 cell via mTOR signaling pathway

Abstract

Objective To explore effects of paclitaxel on proliferation and migration of breast cancer Michigan Cancer Foundation-7 (MCF-7) cells via mammalian target of rapamycin (mTOR) signaling pathway. Methods The cases were randomly divided into four groups, including control group, paclitaxel low-dose group (0.25 μmol/L), paclitaxel medium-dose group (0.5 μmol/L), and paclitaxel high-dose group (1 μmol/L). The viability of MCF-7 cells was measured with methyl thiazolyl tetrazolium (MTT) assay. MCF-7 cell cycle was examined with flow cytometry. MCF-7 cell migration was tested with transwell migration assay. The levels of mTOR signalling pathway-related protein were assayed with Western blot. Results Compared to the control group, MCF-7 cell viability was significantly decreased in paclitaxel low, medium and high-dose groups (P<0.05), and the inhibitory rate was highest at 48 h (P<0.05). MCF-7 cell migration was significantly inhibited in paclitaxel low, medium and high-dose groups [(98±9.78) vs (86.21±6.58), (53.41±3.16) and (42.00±4.69), P<0.05]. Moreover, compared to the control group, the number of MCF-7 cells at G1 phase was significantly increased in paclitaxel low, medium and high-dose groups [(52.14±6.13)% vs (67.93±8.16)%, (72.32±3.67)% and (78.53±6.28)%, P<0.01], the number of MCF-7 cells at G2 phase was significantly reduced in paclitaxel low, medium and high-dose group [(13.68±0.85)% vs (8.57±1.03)%, (5.30±0.89)% and (3.46±0.78)%, P<0.01]. The phosphorylations of 4E binding protein (4EBP1) and mTOR proteins as well as the expressions of cell-cycle protein D1 (Cyclin D1) and matrix metalloproteinase-9 (MMP-9) were significantly inhibited in paclitaxel low, medium and high-dose groups (P<0.01). Conclusions These results suggested paclitaxel could inhibit proliferation and migration in breast cancer MCF-7 cells, which might be related to mTOR signal pathway. Key words: Paclitaxel/AA/PD; Breast neoplasms/DT; Proteins/DE/ME; Signal transduction