METTL16-mediated inhibition of MXD4 promotes leukemia through activation of the MYC-MAX axis.

ABSTRACT: N6-methyladenosine (m⁶A) is an RNA modification that governs multiple aspects of RNA metabolism, including splicing, translation, stability, decay, and the processing of marked transcripts. Although accumulating evidence suggests that the m⁶A writer METTL16 is involved in leukemia, the molecular pathway(s) by which it contributes to leukemogenesis remain unexplored. In this study, we shed light on a novel molecular mechanism whereby METTL16 plays a role in acute myeloid leukemia (AML) progression through an m⁶A-dependent manner. Our investigations revealed that METTL16 is overexpressed in primary AML cells. Genetic depletion of METTL16 or its pharmacological inhibition strongly affected the proliferation of AML cells, eventually triggering apoptosis. Transc

SUBMITTER: Bove G 

PROVIDER: S-EPMC12537489 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature