Transcriptional activator Myb (c-Myb) (MYB)

Transcriptional activator Myb (c-Myb) is a member of the MYB family of transcription factors and is a critical regulator of hematopoiesis, cell proliferation, and differentiation [1, 5, 12]. It functions by binding to specific DNA sequences and recruiting coactivators like p300/CBP to initiate the transcription of genes involved in cell survival and growth [4, 5, 21]. While essential for normal blood cell development, its dysregulation—through overexpression, translocation, or fusion—is a hallmark of several malignancies, including acute myeloid leukemia (AML), adenoid cystic carcinoma (ACC), and breast cancer [3, 10, 15]. In these contexts, MYB acts as an oncogene, driving uncontrolled cell growth and preventing terminal differentiation [1, 6, 10]. Therapeutic strategies currently under investigation include small-molecule inhibitors that disrupt the MYB-p300 interaction, agents that induce the proteasomal degradation of the MYB protein, and RNA-targeted splice modulators [4, 5, 8, 18]. Despite its promise as a target, challenges remain due to its lack of traditional drug-binding pockets and its vital role in maintaining normal hematopoietic stem cells [5, 10, 21].

Other names

c-MybProto-oncogene c-MybMYB proto-oncogenev-myb avian myeloblastosis viral oncogene homologOncogene AMV

Inhibition of transcriptional activity, disruption of protein-protein interaction with coactivators (p300/CBP), induction of proteasomal degradation, and inhibition of gene expression via splice modulation or antisense oligonucleotides [1, 3, 4, 5, 8, 18, 21].