ANGPT1 promotes M1 macrophage polarization and inhibits lung adenocarcinoma progression by inhibiting the TGF-β signalling pathway

Immune cells in the immune microenvironment of lung adenocarcinoma (LUAD) are involved in tumour progression.e aim of this study was to investigate the molecular mechanisms of immune in ltration-related genes in LUAD.e GEO, GeneCards, BioGPS and Genehopper databases were utilized to screen for immune in ltration-related di erentially expressed genes (DEGs) in LUAD.Protein-protein interaction (PPI) network construction and survival analysis were performed in the Kaplan-Meier database to identify hub genes.e TIMER 2.0 database was used to analyse the correlations between hub gene expression and immune in ltration level.Co-culture of LUAD cells with macrophages and plasmid transfection to overexpress ANGPT1 were performed to investigate the function of the hub genes in LUAD using RT-qPCR, Western blot, CCK-8 assays, cell wound healing assays and transwell assays.A total of 88 immune in ltration-related DEGs were screened.e hub genes ANGPT1, CDH5 and CLDN5 were reduced in LUAD, while COL3A1 was overexpressed.ANGPT1 was signi cantly correlated with OS, FP and PPS, and ANGPT1 promoted the polarization of M1 macrophages.Further experiments revealed that ANGPT1 inhibited the proliferation, migration and invasion of LUAD cells by inhibiting the TGF-β signalling pathway.ANGPT1 promotes polarization of M1 macrophages and reduces the progression of LUAD by inhibiting the TGF-β signalling pathway.us, ANGPT1 could be employed as a predictive biomarker and immunotherapy target for lung cancer.