Effect of forkhead box protein P2-mediated activation of myosin light-chain kinase on the invasion and migration of endometrial cancer cells.

OBJECTIVE: Endometrial cancer (EC) ranks among the most prevalent malignant tumors affecting women, with metastasis and dissemination as the major contributors to poor prognosis. This study explores the involvement of forkhead box protein P2 (FOXP2) in EC cell invasion and migration, which is mediated through the activation of myosin light-chain kinase (MYLK). MATERIAL AND METHODS: Bioinformatic analysis was conducted to determine whether FOXP2 is expressed in EC. FOXP2 overexpression was achieved using a FOXP2 overexpression vector (oeFOXP2), and negative control (NC) was used for cell transfection. Cell counting kit-8, 5-ethynyl-2'-deoxyuridine, enzyme-linked immunosorbent assay, colony formation, wound healing, and Transwell assay were used to assess the capabilities of cell viability, invasion, migration, and proliferation. Western blot and quantitative real-time polymerase chain reaction (qRTPCR) analysis were used to measure the expression levels of proteins linked to the epithelial-mesenchymal transition. The correlation between FOXP2 and MYLK was analyzed using bioinformatics and validated by Western blot and qRT-PCR analysis. The MYLK-specific inhibitor ML-7 was employed to study the impact of MYLK-mediated FOXP2 on regulating the malignant biological processes of EC. RESULTS: The oeFOXP2 group of EC cells exhibited a significant decrease in cell viability, colony formation, migration rate, and metastatic cell count compared with the NC group (P < 0.05). FOXP2 overexpression markedly increased caspase-3, caspase-8, caspase-9 activity (P < 0.05). Significant changes were detected in the expression of epithelial-mesenchymal transition marker proteins, with vimentin and N-cadherin expression noticeably declining and E-cadherin expression sharply rising (P < 0.05). The addition of the MYLK-specific inhibitor ML-7 reversed the effect of FOXP2 overexpression on the invasion and migration of EC cells. CONCLUSION: FOXP2 suppresses the proliferation, invasion, and migration of EC cells through the activation of MYLK.