ESCO2-AML Western Blot raw data.pptx

Acute myeloid leukemia (AML) is a prevalent hematologic neoplasms disease. Nucleophosmin (NPM1) encodes a nucleolar chaperone protein, and NPM1 mutation (NPM1c) is the most frequent genetic lesions in AML patients. Cohesin complex functions as a dynamic genomic regulatory machinery regulated by acetyltransferase ESCO2. However, the precise molecular mechanisms by which NPM1c and cohesin dysfunction cooperatively promote AML development remain unclear. Here, we identify ESCO2 as a key modulator in NPM1-mutated AML progression. Overall, this study identifies the interplay between ESCO2 depletion-induced cohesin destabilization and NPM1 mutation in leukemia pathogenesis and reveals a potential therapeutic approach for treating NPM1-mutated AML.