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

T-cell acute lymphoblastic leukemia (T‑ALL) is an aggressive hematological malignancy. The poor prognosis of T‑ALL is closely associated with extensive leukemic infiltration into critical organs. Therefore, the mechanism underlying T‑ALL infiltration is worth investigating. Databases and clinical samples were utilized to examine drebrin 1 (DBN1) expression in T‑ALL. DBN1 knockdown cell lines were established by lentivirus transfection, and cell migration and invasion were examined using Transwell and Matrigel‑Transwell assays. The molecular mechanism was investigated by RNA sequencing and further validated at the molecular level. Reverse transcription‑quantitative PCR and western blotting were employed to examine the expression of downstream molecules following DBN1 knockdown, with subsequent rescue experiments. DBN1‑targeting microRNA (miR) predicted using bioinformatics websites was confirmed using dual‑luciferase assays. In T‑ALL cells, miRNA mimics transfection enabled functional validation, and investigations into the underlying molecular mechanisms encompassing rescue experiments. Clinical samples and publicly available databases revealed that DBN1 was upregulated in patients with T‑ALL patients. DBN1 knockdown significantly decreased the migration and invasion of T‑ALL cells