DBN1‑mediated upregulation of GAB2 facilitates the migration and invasion of T‑cell acute lymphoblastic leukemia cells

. RNA sequencing revealed that downregulation of DBN1 could reduce Grb2‑associated binding protein 2 (GAB2) expression. Western blotting revealed that GAB2 expression, and PI3K/AKT and MAPK/ERK signaling were decreased in DBN1‑knockdown cells. GAB2 overexpression restored the phosphorylation of downstream effectors (AKT and ERK1/2). Bioinformatics and dual‑luciferase reporter experiments identified miR‑218‑5p binding to the 3'-untranslated region of DBN1, which suppressed DBN1 expression. In addition, the experiments demonstrated that miR‑218‑5p acted as an upstream regulator of DBN1, and was involved in cell migration and invasion. Overall, DBN1 was upregulated in T‑ALL, and its depletion inhibited cell migration and invasion through downregulation of GAB2 and consequent inhibition of AKT and ERK signaling cascades. The present data suggested that DBN1 could be a novel biomarker of T‑ALL infiltration, which is a novel perspective in the field of leukemia research.