Ginsenoside-Rh2 inhibits U251 glioma cell migration and invasion via the Gab2/Akt2 pathway

Glioma, the most common primary intracranial tumor, exhibits high recurrence and mortality rates. Ginsenoside-Rh2 (GS-Rh2), an active compound from Panax ginseng, has shown anti-tumor potential. Gab2, a tyrosine kinase substrate, is implicated in glioma pathogenesis; however, the mechanism by which GS-Rh2 might inhibit glioma cell migration and invasion via the Gab2/Akt2 pathway remains unexplored.

To investigate the effects and mechanisms of GS-Rh2 on glioma cell migration and invasion through the Gab2/Akt2 signaling pathway.

U251 glioma cells were treated with GS-Rh2 in vitro. Cell viability was assessed by MTT assay. Western blot was used to detect Gab2 and p-Akt2 expression. In vivo, GS-Rh2 was administered to nude mice bearing U251 or siGab2/U251 intracranial xenografts. HE staining assessed brain invasion, and western blot detected Gab2 and Akt2 expression in tumor tissues.

GS-Rh2 significantly inhibited U251 cell proliferation, migration, and invasion both in vitro and in vivo (P < 0.05), while no significant effects were observed in siGab2/U251 cells. At the molecular level, GS-Rh2 significantly reduced Gab2 expression and Akt2 phosphorylation in U251 cells and brain tumor tissues (P < 0.05).

GS-Rh2 inhibits migration and invasion of U251 glioma cells by decreasing Gab2 expression and Akt2 phosphorylation, suggesting that GS-Rh2 targets the Gab2/Akt2 signaling axis.