Resveratrol (RES) has been found to inhibit the progression of lung cancer. Our study aims to explore the molecular mechanisms by which RES regulates lung adenocarcinoma (LUAD) progression. Our study unveils two key novel findings: First, our study demonstrates that EPHB2 is a direct functional target of RES in LUAD. Molecular docking and CETSA confirmed the binding, and crucially, EPHB2 overexpression reversed the anti-tumor effects of RES. Second, our study reveals a previously unrecognized role for EPHB2 in promoting glycolysis in LUAD, which is effectively suppressed by RES. Specifically, RES potently inhibited LUAD tumor growth in vivo and suppressed cell proliferation, migration, invasion, and glycolysis in vitro . These inhibitory effects were consistently abolished upon EPHB2 overexpression. Collectively, our findings suggest that RES inhibits LUAD cell proliferation, migration, invasion, and glycolysis, with EPHB2 downregulation appearing to contribute to these effects. Further studies are needed to determine whether RES directly targets EPHB2 and to evaluate the translational potential of these findings.
Chen et al. (Sun,) studied this question.