LGR6 promotes the progression of gastric cancer through PI3K/AKT/mTOR pathway.

Abstract

BackgroundIn the present study, we aimed to investigate the role of LGR6 in the progression of gastric cancer (GC) and explore the intrinsic molecular mechanisms.Materials and methodsThe lentiviral LGR6 shRNA (sh-LGR6) and lentiviral expression vector of LGR6 gene (OE-LGR6) were used to regulate the LGR6 expression. Furthermore, we performed in vitro experiments to observe whether PI3K/AKT/mTOR pathway was affected by LGR6 and assess the role of LGR6 in the proliferation, apoptosis, migration, and invasion of GC cells.ResultsOur data showed that phosphorylated AKT and mTOR were downregulated by sh-LGR6 (P<0.05). The expressions of proapoptotic proteins Bax and Caspase-3 were upregulated by sh-LGR6 (P<0.05); the expression of antiapoptotic protein Bcl2 was downregulated by sh-LGR6 (P<0.001). Besides, the functional experiments proved that sh-LGR6 could promote the apoptosis of GC cells and inhibit the proliferation, invasion, and migration of GC cells (P<0.001). Compared with sh-LGR6, OE-LGR6 led to the opposite results.ConclusionLGR6 is an antiapoptosis protein which controls the progression of GC through PI3K/AKT/mTOR pathway. More in vivo experiments and clinical trials are necessary to confirm the possibility of LGR6 in tumor therapy.