CEP131 knockdown inhibits cell proliferation by inhibiting the ERK and AKT signaling pathways in non-small cell lung cancer.

Abstract

Disrupted centrosome-associated family protein expression can result in the detrimental duplication of centrosomes, causing genomic instability and subsequent carcinogenesis. Limited research has demonstrated that centrosomal protein 131 (CEP131) exhibits oncogenic activity in osteosarcoma, hepatocellular carcinoma and breast cancer. The present study demonstrated that there is an association between CEP131 expression and advanced Tumor-Node-Metastasis stage (P=0.016), and positive regional lymph node metastasis (P=0.023) in 91 cases of non-small cell lung cancer. A549 and SPC-A-1 cells, with moderate expression levels of CEP131, were selected as representative cell lines. The results indicated that downregulation of CEP131 induced G1/S cell cycle arrest, inhibition of cyclins D1/E and cyclin-dependent kinases 2/4/6, and induction of inhibitory p21/p27, all of which are regulated by ERK and AKT signaling, suggesting that CEP131 exhibits potential as a novel target in the treatment of lung cancer.