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.

Serine Incorporator 2 (SERINC2) Expression Predicts an Unfavorable Prognosis of Low-Grade Glioma (LGG): Evidence from Bioinformatics Analysis

“…Player and colleagues reported the differential distribution of SERINC2 in normal human tissues (Player et al 2003 ), and the transcript level of SERINC2 was the highest in the bladder, kidney, and muscle but was undetectable in the brain, spleen, and heart. Our understanding of the role of SERINC2 in cancer is limited and requires further investigation (Zeng et al 2018 ).…”

“…Ren et al (Ren et al 2014 ) reported that the downregulation of SERINC1 expression resulted in impaired cell cycle progression of hepatocellular carcinoma. Zeng et al (Zeng et al 2018 ) found that SERINC2 knockdown inhibited lung adenocarcinoma proliferation, migration, and invasion but without significant differences in the cell cycle. The present study focused on the possible pathways of SERINC2 correlation genes and further analyzed the correlation genes using GO term and KEGG pathway analyses.…”

“…Interference with distinct steps of sphingolipid synthesis and signaling attenuates the proliferation of glioma cells (Bernhart et al 2015 ). Knockdown of SERINC2 inhibits the proliferation, migration, and invasion in lung adenocarcinoma (Zeng et al 2018 ). Kainite-induced seizures rapidly upregulates SERINC2 in neuronal cell layers of the rat hippocampus (Ren et al 2014 ).…”

Long noncoding RNA MEG3 plays a promoting role in the proliferation, invasion, and angiogenesis of lung adenocarcinoma cells through the AKT pathway

“…A majority of recent studies concerning the role of MEG3 in tumors imply that MEG3 acts as a tumor inhibitor in cancers. Particularly in the lung adenocarcinoma field, Lu et al proposed that MEG3 was significantly downregulated in non–small‐cell lung cancer (NSCLC) tissues and that MEG3 regulated NSCLC cell proliferation and apoptosis via the activation of p53 . In addition, Liu et al demonstrated that MEG3 is significantly downregulated in lung adenocarcinoma and partially regulates the cisplatin resistance of lung adenocarcinoma cells through the control of p53 and Bcl‐xl expression.…”

“…3.4 | The overexpression of MEG3 promotes lung adenocarcinoma through the AKT pathway It has been reported that the aberrant activation of the AKT pathway are often related with the lung adenocarcinoma cell proliferation, migration, invasion, and angiogenesis [8][9][10][11] In this paper, we surmised that MEG3 might regulate cell proliferation, migration, invasion, and angiogenesis by activating the AKT pathway in lung adenocarcinoma. The results of Western blot analysis showed that the overexpression of MEG3 led to the increase in phosphorylated F I G U R E 4 MEG3 overexpression promotes the angiogenesis of lung adenocarcinoma.…”