FOXM1 promotes TGF-β2-induced injury of human lens epithelial cells by up regulating VEGFA expression

Objective To explore whether Fork head box protein M1 (FOXM1) is involved in TGF-beta 2-induced injury of human lens epithelial cells and its related mechanism. Methods Human lens epithelium samples from cataract patients and healthy controls were collected. A cellular epithelial injury model was established by treating HLE-B3 cells with TGF-beta 2. QPCR, immunoblot assays were performed to detect the levels of FOXM1 in human cataract samples and the lens epithelial injury cell model. FOXM1 siRNA and pcDNA3.1-FOXM1 plasmids were transfected into the cells to knockdown and overexpress FOXM1, respectively. MTT and wound closure and transwell assays were performed to analyze cell proliferation and migration in HLE-B3 cells. Immunoblot assays were also conducted to detect the effects of FOXM1 on EMT, VEGFA and MAPK/ERK signaling. Results We found high expression of FOXM1 in lens tissues of cataract patients. Silencing of FOXM1 in TGF-beta 2-induced HLE-B3 cells suppressed cell proliferation, migration, and the EMT process. Mechanistically, we found that downregulation of FOXM1 inhibited the VEGFA/MAPK signaling pathway in TGF-beta 2-induced HLE-B3 cells. Conclusion FOXM1 promoted TGF-beta 2-induced injury of human lens epithelial cells (hLECs) by promoting VEGFA expression. FOXM1 could be a potential drug target for the treatment of ocular diseases.