RFTN1 facilitates gastric cancer progression by modulating AKT/p38 signaling pathways

Gastric cancer (GC), a malignant tumor originating from the epithelium of the gastric mucosa, has been endangering human health for many years. The current standard surgical resection is not ideal for advanced gastric cancer. Therefore, it is urgent to find new prognostic indicators as well as drug targets. In our study, referring to clinicopathological characteristics of GC, we found that raftlin lipid raft linker 1 (RFTN1) had high expression in primary GC tissues. Subsequently, we showed that knockdown of RFTN1 inhibited GC cell proliferation and induced cell cycle arrest in G0/G1 phase, and promoted GC cell apoptosis. Conversely, overexpression of RFTN1 promoted GC cell proliferation and G0/G1 to S phase transition, and inhibited apoptosis. Furthermore, cell derived xenograft experiments showed that knockdown of RFTN1 inhibited GC cell growth in vivo. Notably, our experimental data demonstrated that knockdown of RFTN1 could inhibit the AKT signaling pathway and activate p38 signaling pathway, whereas overexpression of RFTN1 did the opposite. Moreover, the effects caused by knockdown of RFTN1 in GC cells could be rescued by using SC79 (an AKT activator). In conclusion, these results indicated that RFTN1 plays an oncogenic role in GC, and might act as a prospective prognostic indicator or therapeutic target for GC patients.