Leukemia Research
Volume 36, Issue 5 , Pages 607-618, May 2012

Proteomic analysis identifies differentially expressed proteins in AML1/ETO acute myeloid leukemia cells treated with DNMT inhibitors azacitidine and decitabine

Functional Unit of Hematology, University of Florence, Florence, Italy

Received 5 August 2011; received in revised form 28 October 2011; accepted 29 November 2011. published online 10 January 2012.

Abstract 

Azacitidine and decitabine are DNA methyltransferase inhibitors used to treat myelodysplastic syndromes and acute myeloid leukemias. To further characterize different mechanisms between these two agents, cellular extracts from leukemic cells untreated or treated with either drug were analyzed using 2D electrophoresis. Numerous differentially expressed proteins were identified with MALDI-TOF/TOF-MS. Cyclophilin A, Catalase, Nucleophosmin and PCNA were decreased exclusively by azacitidine, TCP1 and hnRNP A2/B1 by both drugs; alpha-Enolase and Peroxiredoxin-1 by decitabine. Interestingly, the expression of the proinflammatory protein Cyclophilin A, also suggested as marker of cell necrosis, was stimulated by decitabine. Finally, a comprehensive pathway analysis of data highlighted a relationship between the identified proteins and potential effectors.

Keywords: AML, Proteomics, Azacitidine, Decitabine

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PII: S0145-2126(11)00577-7

doi:10.1016/j.leukres.2011.11.024

Leukemia Research
Volume 36, Issue 5 , Pages 607-618, May 2012

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