TSPAN8 regulates EGFR/AKT pathway to enhance metastasis in gastric cancer

BackgroundTetraspanin 8 (TSPAN8), a transmembrane glycoprotein, is implicated in various pathological conditions including human malignancies. However, the roles and underlying mechanisms of TSPAN8 in promoting gastric cancer(GC) progression are yet to be fully understood.Methods and resultsOur study found that TSPAN8 expression was significantly elevated in GC tissues. We also observed a positive correlation between high TSPAN8 expression and various clinicopathological characteristics of GC, including tumor differentiation, invasion depth, lymph node metastasis, and clinical stage. Moreover, the elevated TSPAN8 expression was indicative of poor prognosis. Functionally, we observed that knockdown of TSPAN8 significantly attenuated while overexpression of TSPAN8 promoted GC cell migration and invasion. In vivo experiments, knockdown of TSPAN8 suppressed lung metastasis in nude mice. We further explored the underlying mechanisms of TSPAN8 and found that it regulated EGFR expression in GC cells by accelerating phosphorylation of EGFR and AKT.ConclusionsOur study reveals that TSPAN8 plays a significant role in promoting tumor metastasis by activating the EGFR/AKT pathway, indicating that it may serve as a promising therapeutic target of gastric cancer.

Automated summary

This study reveals that TSPAN8 is significantly upregulated in gastric cancer tissues and is associated with clinicopathological characteristics and poor prognosis. TSPAN8 promotes cancer cell migration and invasion by activating the EGFR/AKT pathway and regulating EGFR expression. Therefore, TSPAN8 may serve as a promising therapeutic target for gastric cancer.