Abstract:
Objective This study aimed to investigate the inhibitory effects of paclitaxel and cisplatin against the triple-negative breast cancer cell line HCC1937 in vitro, and to explore the underlying mechanisms in relation to the MAPK signaling pathway.
Methods A Cell Counting Kit-8 assay was used to detect the 50%inhibitory concentration(IC50) of paclitaxel and cisplatin on HCC1937 and MCF-7 cells.Flow cytometry and Western blot analysis were used to determine the cell cycle distribution and MAPK signaling pathway protein expression after incubating the HCC1937cells with paclitaxel or cisplatin for 48 h.
Results The HCC1937 cells were significantly more sensitive to cisplatin(IC50= 6-9μg/ml) than MCF-7 cells(IC50= 18-20μg/ml)(P < 0.01), whereas the HCC1937 cells were less sensitive to paclitaxel(IC 50= 3-4.6μg/ml) than the MCF-7 cells(IC50 = 0.12-0.3μg/ml)(P < 0.01).Paclitaxel caused the MCF-7 cells to arrest at the G 2/M phase in a concentration-dependent manner, whereas cisplatin acted by arresting cells at the G0/G1 phase.P-JNK and P-P38 protein expression significantly increased after the cells were treated with the two drugs for 48 h compared with the control group.However, P-ERK protein expression in the cisplatin group was significantly lower than in the control group for the HCC1937cells.
Conclusion HCC1937 cells have higher chemosensitivity to cisplatin than to paclitaxel.Paclitaxel and cisplatin can both activate the JNK/SAPK and P38 signaling pathways in HCC1937 cells, whereas different cisplatin concentrations can inhibit the activation of the ERK signaling pathway.