Background: In 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 methods: The 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.
Results: Our 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.
Conclusion: LGR6 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.
Keywords: LGR6, pathway, tumor therapy, gastric cancer