Promotion of non-small cell lung cancer tumor growth by FHL2 via inducing angiogenesis and vascular permeability

Antiangiogenetic therapy is one of the effective strategies for non-small cell lung cancer (NSCLC) treatment. Four-and-a-half LIM-domain protein 2 ( ) serves as a key function in cell growth and metastasis of multiple cancers, but the role of in NSCLC angiogenesis has not been intensely examined. expression in NSCLC tissues and cell lines and its correlation with patients prognosis were investigated by using The Cancer Genome Atlas (TCGA) database and quantitative polymerase chain reaction (qPCR). Cell Counting Kit-8 (CCK-8) assay, EdU (5-ethynyl-2'-deoxyuridine) assay, and a xenograft model were used to investigate the effects of on NSCLC progression and . CCK-8, wound-healing, Transwell invasion, tube formation, and permeability assays were performed to determine the roles of in angiogenesis and vascular permeability. Vascular endothelial growth factor A (VEGFA) enzyme-linked immunosorbent assay (ELISA) assay, Western blot analysis, and MK-2206 were used to investigate the specific mechanism mediated by . We demonstrated that was significantly upregulated in NSCLC tissues and cell lines and was associated with poor prognosis. overexpression enhanced the cell viability of NSCLC cells, as well as the proliferation, migration, invasion, and tube formation of human umbilical vein endothelial cells (HUVECs). In addition, we determined that activated the AKT-mTOR signaling pathway in HUVECs by promoting VEGFA secretion from NSCLC cells, thereby inducing angiogenesis and vascular leakiness. We further confirmed that also promoted NSCLC tumor growth . Our study revealed the role of in NSCLC and the mechanism by which promotes NSCLC tumorigenesis, providing novel insights into targeted therapy for NSCLC.