NCAPG-mediated CDK1 promotes malignant progression of non-small cell lung cancer via ERK signaling activation.

Abstract

Non-SMC condensing I complex subunit G (NCAPG) has been implicated in tumor progression. However, its role, potential mechanism and prognostic significance in human non-small cell lung cancer (NSCLC) remain elusive. Through the conjoint analysis of the TCGA and The Gene Expression Omnibus (GEO) databases, we confirmed that NCAPG is an upregulated gene. The prognostic value of NCAPG was elucidated through data analysis. The functional roles and mechanistic insights of NCAPG in NSCLC growth and metastasis were evaluated in vitro and in vivo. NCAPG expression was significantly increased in NSCLC. Multivariate Cox regression analysis demonstrated that NCAPG was an independent prognostic factor in patients with NSCLC. The high expression of NCAPG was significantly correlated with lymphatic metastasis. Additionally, the high expression of NCAPG effectively promoted the growth and metastasis of NSCLC in vitro and in vivo. In terms of mechanism, the interaction between NCAPG and Cyclin-dependent kinase 1 (CDK1) promotes the phosphorylation of Extracellular signal-regulated kinase (ERK). Overall, our results reveal the key role of NCAPG in NSCLC and highlight the regulatory function of the NCAPG/CDK1/ERK axis in regulating the progression of NSCLC, providing potential prognosis and therapeutic targets for the treatment of NSCLC.