Downregulation of SDCBP inhibits cell proliferation and induces apoptosis by regulating PI3K/AKT/mTOR pathway in gastric carcinoma

Syndecan-binding protein (SDCBP) has been reported to critically process a core role in tumorigenesis. This study was conducted to characterize a novel regulatory network of SDCBP in gastric carcinoma (GC) cells. Our findings indicated that overexpression of SDCBP promoted the proliferation of GC cell and increased proliferating cell nuclear antigen (PCNA) expression. Moreover, the overexpression of SDCBP suppressed the apoptosis of GC cell along with a decrease of Bax/Bcl-2 ratio and induction of PI3K/AKT/mTOR activation. However, knockdown of SDCBP exhibited opposed effects on GC cells. Furthermore, silencing SDCBP significantly inhibited GC cell viability and PCNA expression accompanied with the upregulated cell apoptosis and Bax/Bcl-2 ratio, which was regulated by PI3K/AKT/mTOR signaling pathway. And it was further determined that PI3K inhibitor LY294002, AKT inhibitor Torin1, and mTOR inhibitor MK-2206 suppressed the apoptosis. In conclusion, SDCBP promotes the growth ability of GC by inducing the PCNA expression and inhibiting GC cell apoptosis via inactivation of the PI3K/AKT/mTOR pathway.