Selective HDAC6 inhibitor WT161 modulates the VLA-4/FAK pathway by inhibiting PKA activity in acute lymphoblastic leukemia.

ABSTRACT: Acute lymphoblastic leukemia (ALL) is a genetically heterogeneous malignancy often associated with poor prognosis due to chemotherapy resistance and relapse. Histone deacetylase (HDAC) inhibitors represent an emerging class of epigenetic antitumor drugs. Among them, HDAC6, which is an enzyme that deacetylates α-tubulin, is increasingly recognized as a potential therapeutic target in hematologic malignancies. The adhesion molecule very late antigen 4 (VLA-4) plays a key role in cell adhesion-mediated drug resistance (CAMDR). We hypothesized that inhibiting HDAC6 could counteract CAMDR mediated by crosstalk between α-tubulin and integrin signaling. This study therefore investigated the therapeutic potential of WT161, a selective HDAC6 inhibitor, focusing on its role in targeting of the VLA-4

SUBMITTER: Lv C 

PROVIDER: S-EPMC12624111 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature