Expression and relationship of ECT2 with cell cycle proteins CDK1 and CyclinB1 on the Paclitaxel intervention in three negative breast cancer cells

Abstract Purpose To investigate the relationship of expression of ECT2 and cell cycle-related proteins CDK1 and CyclinB1 in triple-negative breast cancer cells (TNBC) after ECT2 overexpression and interference and after paclitaxel (PTX) therapy,and hope to provide some theoretical basis for the treatment of TNBC Methods ECT2 overexpression and interfering plasmid were applied to cultured TNBC HCC1806 cells and nude mouse transplantation tumor assays were performed, while PTX was added in the group, and Westen-blot detected the expression of ECT2, CDK1, and CyclinB1 proteins.The relationship between the ECT2 and CDK1 and CyclinB1 genes was analyzed by TCGA database. Results In vitro experiments,The ECT2 overexpression group showed that ECT2 protein expression was higher than that of the control group before and after PTX treatment ( P < 0.05), and CDK1 and Cyclin B1 was similarly higher than the control group ( P < 0.05), but the three proteins after PTX treatment was lower than that before.The ECT2 interference group showed that the expression of ECT2 and CDK1 and Cyclin B1 was lower than that of the control group ( P < 0.05), especially after PTX treatment, the decrease of their expression was more significant. In vivo experiments,the expression of ECT2 was significantly higher in the overexpression group and the overexpression group with the addition of PTX than control group ( P < 0.05), and significantly lower in the PTX group, the interference group and the interference group with the addition of PTX than control group ( P < 0.05),and CyclinB1 protein expression was statistically different in the ECT2 overexpression group and interference group with the addition of PTX compared with the PTX control group ( P < 0.05).The results of the TCGA database analysis showed that there was a positive correlation between the ECT2 and CDK1 and CyclinB1 genes. Conclusion ECT2 promotes TNBC cell progression by acting in the G2/M phase of the cell cycle, and it may form a positive feedback loop with Cyclin B1 to promote the progression of the cell cycle and accomplish cell proliferation under the regulation of CDK1. The overexpression of ECT2 may cause TNBC resistance to PTX,and combination of anti-ECT2-targeted drugs and PTX may offer help in TNBC treatment.