BCAT1 is up-regulated in lung adenocarcinoma tissues and promotes cell proliferation and metastasis through NF-kB pathway activation

BCAT1 is up-regulated and acts as an important oncogenic factor in many types of cancers, but its role in lung adenocarcinoma (LUAD) development is not clearly understood. Here we investigated the function and mechanism of BCAT1 in LUAD progression. In this study, we found BCAT1 was up-regulated in tumor tissues, and its expression level was associated with TNM stage and local lymph node metastasis of LUAD patients. Besides, BCAT1 knockdown inhibited cell growth and mobility, while BCAT1 overexpression promoted LUAD development both in vitro and in vivo. Bioinformatics analysis of RNA sequencing results suggested that differentially expressed genes (DEGs) in BCAT1 overexpression LUAD cells were mainly associated with cancer development, which were enriched in metabolism, signal transduction, and immune response processes. Among the DEGs, decreased mRNA level of NFKBIB indicated NF-kB pathway activation. Furthermore, as an inhibitor of NF-kB pathway, ammonium pyrrolidinedithiocarbamate (PDTC) treatment could predominately counteract the effect of NF-kB pathway activation and inhibited LUAD cells proliferation and migration, especially cells with BCAT1 overexpression. Taken together, our findings point a key role for BCAT1 in promoting LUAD development through NF-kB pathway activation, which provides promising molecular biomarker and therapeutic targets for LUAD diagnosis and treatment.