SERINC2-knockdown inhibits proliferation, migration and invasion in lung adenocarcinoma.

Abstract

Serine incorporator 2 (SERINC2) is a member of the SERINC family of transmembrane proteins that incorporate serine into membrane lipids during synthesis. In the present study, the biological function of SERINC2 in lung adenocarcinoma cells was investigated. The data from a previous study and the publicly available Oncomine database were analysed regarding the expression levels of SERINC2 mRNA in lung adenocarcinoma. A lentiviral-based short hairpin RNA (shRNA) was used to suppress SERINC2 expression in lung cancer cells. The effect of SERINC2 expression on lung cancer proliferation was determined using cell counting kit-8 and colony formation assays. The influence on invasion and migration was examined in vitro using Transwell and wound-healing assays, respectively. Phosphorylated protein kinase B (p-AKT) expression levels were assessed by immunoblotting. According to a previous study and Oncomine, expression levels of SERINC2 mRNA are significantly upregulated in tumour tissues compared with those in healthy tissues in patients with lung adenocarcinoma. SERINC2-knockdown by lentiviral-based shRNA inhibited the proliferation, migration and invasion of the H1650 and A549 cells. In addition, p-AKT expression levels were significantly decreased following SERINC2-knockdown. In conclusion, SERINC2-knockdown suppresses lung adenocarcinoma proliferation, migration and invasion through a mechanism that may be associated with phosphatidylinositol 3-kinase/AKT signalling. Based on these findings, SERINC2 serves an important role in the progression of lung adenocarcinoma.