Effect of ECT2 Gene on Proliferation of Cervical Cancer Cells and Its Mechanism

Objective To study the effect of epithelial cell transformation sequence 2 (ECT2) on the proliferation of cervical cancer cells and its mechanism.

Methods We transfected cervical cancer cells HeLa (HeLa-ECT2) with the lentivirus overexpressing ECT2 and the cells SiHa (SiHa-siRNA) and C33a (C33a-siRNA) with the interfering plasmid. MTT assay was performed to detect cell proliferation ability. Flow cytometry was conducted to detect the cell cycle of each group. The IPA database was searched for the interacting proteins of ETC2, and immunofluorescence subcellular localization verified the effect between the two. qPCR and Western blot were carried out to detect the expression of Rac1, Cdc42, CDK1, and Cyclin B1 mRNA and protein in each group of cells.

Results ECT2 may interact with CDK1. After ECT2 expression was upregulated, the G₂/M phase of HeLa-ECT2 cells accelerated the transformation to G₁ phase, cell proliferation ability was enhanced, and the expression levels of Rac1, Cdc42, CDK1, and cyclin B1 mRNA and protein all increased (P < 0.001); the knockdown of ECT2 expression would reverse the effect (P < 0.05).

Conclusion ECT2 accelerates G₂ phase of cervical cancer cells to G₁ phase and promotes cell proliferation by co-localizing with CDK1 through the downstream Cdc42/Rac1 signaling pathway.