The mechanism study of Eag1 potassium channel in gastric cancer.

Abstract

Heredity factors may play a vital role in gastric cancer (GC) progression. This study is aimed to explore and validate the influence and the role of Eag1 on the susceptibility to GC. The successfully constructed Ad5-Eag1-shRNA vector was transfected into GC cells [SGC-7901 and BGC-823, short hairpin RNA (shRNA) group]. Reverse transcription polymerase chain reaction (RT-PCR) and western blotting were conducted for assessment of Eag1 messenger RNA (mRNA) and protein expression levels. Cell proliferation and cell colony formation was measured by Cell Counting Kit-8 (CCK-8) assays. Flow cytometry was performed for cell cycle progression assessment. Bioinformatic analysis was analyzed for Eag1 validation with multiple public databases. The expression of Eag1 was significantly down-regulated in the shRNA group in comparison with the empty vector and control groups (P<0.05). Cell proliferation rate and clone formation number were lower in the shRNA group, and a decreased cell proportion in G2-S phase and an increased proportion in G1-G0 were observed in the shRNA group (P<0.05). When transfected with Ad5-Eag1-shRNA, cyclin D1 and cyclin E protein expression were inhibited. Bioinformatic analysis showed that Eag1 expression was strongly associated with the prognosis and immune infiltration of GC. The Eag1 gene may affect occurrence and development of GC through regulating cyclin D1 and cyclin E expression.