Loss of FGL1 induces epithelial-mesenchymal transition and angiogenesis in LKB1 mutant lung adenocarcinoma

Liver kinase b1 (LKB1) is a tumor suppressor, and the inactivated mutation frequency of LKB1 in lung adenocarcinoma is 20%. The present study aimed to explore potential novel biomarkers in LKB1 mutant lung adenocarcinoma. Gene expression data from lung adenocarcinoma patients were downloaded from The Cancer Genome Atlas and the Gene Expression Omnibus databases. R software was used to analyze the gene expression profiles. Reverse transcription-quantitative PCR (RT-qPCR), western blot and immunohistochemistry (IHC) analyses were used to examine gene expression and function. Gene function was further explored via gene set enrichment analysis. A colony formation assay was used to evaluate cell proliferation. A wound-healing assay and immunofluorescence analysis were used to evaluate cell migration and epithelial-mesenchymal transition (EMT), respectively. Wound healing assay, immunofluorescence, western blot, RT-qPCR and IHC results for EMT-associated markers demonstrated that a loss of fibrinogen-like 1 (FGL1) induced EMT in LKB1 mutant lung adenocarcinoma. RT-qPCR and IHC analyses of angiogenesis-related markers revealed that loss of FGL1 promoted angiogenesis in LKB1 mutant lung adenocarcinoma. Overall, the present results demonstrated that loss of FGL1 induced EMT and angiogenesis in LKB1 mutant lung adenocarcinoma. FGL1 may be a novel biomarker to indicate EMT and angiogenesis in patients with LKB1 mutant lung adenocarcinoma.