FOXM1 promotes TGF-beta 2-induced injury of human lens epithelial cells by up regulating VEGFA expression
作者全名:"Li, Xuemei; Gao, Wei; Zhang, Yanlai"
作者地址:"[Li, Xuemei; Gao, Wei] Kashgar Prefecture Second Peoples Hosp, Dept Ophthalmol, Kashgar 844000, Xinjiang, Peoples R China; [Zhang, Yanlai] Chongqing Med Univ, Dept Ophthalmol, Chongqing Eye Inst, Chongqing Branch,Natl Clin Res Ctr Ocular Dis,Affi, 1 Youyi Rd, Chongqing, Peoples R China"
通信作者:"Zhang, YL (通讯作者),Chongqing Med Univ, Dept Ophthalmol, Chongqing Eye Inst, Chongqing Branch,Natl Clin Res Ctr Ocular Dis,Affi, 1 Youyi Rd, Chongqing, Peoples R China."
来源:GRAEFES ARCHIVE FOR CLINICAL AND EXPERIMENTAL OPHTHALMOLOGY
ESI学科分类:CLINICAL MEDICINE
WOS号:WOS:000975510700001
JCR分区:Q2
影响因子:2.4
年份:2023
卷号:
期号:
开始页:
结束页:
文献类型:Article; Early Access
关键词:Cataract; Fork head box protein M1 (FOXM1); Transforming growth factor-beta 2 (TGF-beta 2); HLE-B3; VEGFA/MAPK pathway
摘要:"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."
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