GSE75401
Gene expression profiling of the MLL-AF9 induced AML cells (wild type and Dnmt3b-KO)
Acute myeloid leukemia (AML) is a heterogeneous hematopoietic disorder with a poor prognosis. Abnormal DNA methylation is involved in the initiation and development of AML. The de novo methyltransferases Dnmt3a and Dnmt3b are responsible for the generation of genomic methylation patterns. While DNMT3A is frequently mutated in hematologic malignancies, DNMT3B is rarely mutated. To investigate the role of Dnmt3b in AML, we genetically inactivated Dnmt3b in an MLL-AF9 induced AML mouse model. Gene profiling using a microarray revealed the upregulation of the oncogenic gene set and the downregulation of the cell differentiation gene set. Our results indicate that Dnmt3b plays the role of a tumor suppressor in MLL-AF9 AML progression, which reveals new insights into the roles of DNA methylation in leukemic development. Overall design: Microarray experiments were conducted for 6 samples, including three control leukemia cells and three Dnmt3b knockout (KO) leukemia cells sorted from the BM of leukemia recipient mice.