Aberrant expression of JAM2 inhibits invasion and migration in lung adenocarcinoma

Abstract Purpose: lung adenocarcinoma (LUAD) is the most prevalent histologic subtype in lung cancer. As a number of Junctional adhesion molecule (JAM) family, JAM2 involves in multiple functions, such as cell-cell contacts, as well as tumor development. Different expression profiles and roles of JAM2 have also been studied in various cancers. However, the clinical and biological significance of JAM2 in LUAD has not been fully illuminated. Methods: Four gene expression profiles were downloaded from the Gene Expression Omnibus database (GEO) to identify differentially expressed genes (DEGs) between LUAD and normal tissure. Then, GEPIA was employed to unveil expression level and prognosis value of JAM2 in LUAD. Enrichment analyses were performed among coexpression genes in different JAM2 subgroups. Moreover, a protein-protein interaction (PPI) network of the coexpression genes was constructed, and hub genes were explored with Cytoscape software. The expression of JAM2 was verified in LUAD cell lines, wound-healing assays and transwell assays were used to identify cell migration and invasion abilities.Results: we confirmed that JAM2 was downregulated in LUAD, which may be the result of methylation. JAM2 could be served as an independent prognostic gene to predict the outcomes of LUAD patients. It played a broad role in LUAD inflammatory infiltration and higher JAM2 expression may predict a better immunotherapy response. What’s more，we found migratory and invasive capabilities of LUAD cells were significantly suppressed when JAM2 was overexpressed. Conclusion: According to the findings, JAM2 may be a promising molecular target for early diagnose and targeted therapy of LUAD.