Increased expression of NCAPG (Non-SMC condensing I complex subunit G) is associated with progression and poor prognosis of lung adenocarcinoma.

Recently, studies have shown that the up-regulation of Non-SMC Condensin I Complex Subunit G (NCAPG) in some tumors can promote tumor progression, and its high expression has a strong correlation with the poor prognosis of patients. However, there are few studies on NCAPG in lung adenocarcinoma (LUAD). Our research is to explore the role of NCAPG in LUAD and try to reveal the possible molecular mechanism. We use public databases and tissue samples from LUAD patients to verify that NCAPG is significantly up-regulated in LUAD, and the high expression of NCAPG is related to the poor prognosis of patients. Subsequently, we found that silencing NCAPG can inhibit the proliferation and invasion of LUAD cells in vitro and the growth of subcutaneous tumors in nude mice in vivo. In order to explore the possible molecular mechanism of NCAPG's function, we found out the genes co-expressed with NCAPG through the cBioportal database, and discovered that these genes were significantly enriched in the cell cycle and other pathways through DAVID analysis, which implies the importance of NCAPG in the cell cycle. Finally, we confirmed by flow cytometry that NCAPG affects the conversion of cell cycle mitosis from G1 to S. Taken together, our research results suggest that NCAPG plays a role in the progress of LUAD. Moreover, NCAPG can be used as a potential biomarker for the diagnosis of LUAD, as well as a potential therapeutic target for patients with LUAD.