Acute myeloid leukemia (AML) is a type of blood malignancies with high genetic heterogeneity. Epigenetic alterations including histone acetylation have been found to be the key genetic variations driving the occurrence of AML. However, targeting histone acetylation remains to be unsuccessful in leukemia therapy. Recently, acidic nuclear phosphoprotein 32 family member A (ANP32A) was shown to be a novel biomarker of unfavorable outcome for leukemia and promote AML by stimulating histone 3 (H3) acetylation and the abnormal expression of lipid metabolism genes. A small peptide that competitively binds to H3 to block the interaction of ANP32A and H3 exhibited therapeutic effect in vitro and in vivo. Here, we further explore the potential anti-leukemia strategy by targeting ANP32A that consequently lead to alteration of H3 acetylation. In view of the therapeutic significance of targeting ANP32A in AML, the intervention tactics as well as its clinical perspectives and challenges will be adequately discussed.
ANP32A, AML, H3 Acetylation, H3BP, Targeted intervention