Abstract
BACKGROUND: 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. METHODS: 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. RESULTS: 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 G(2)-S phase and an increased proportion in G(1)-G(0) 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. CONCLUSIONS: The Eag1 gene may affect occurrence and development of GC through regulating cyclin D1 and cyclin E expression.