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Gene expression profiles in mouse common myeloid progenitor (CMP) and leukemia cells expressing full-length MN1 or truncated versions of MN1 protein

ABSTRACT: We used Affymetrix microarrays to characterize gene expression profiles that were perturbed in common myeloid progenitor (CMP) cells due to enforced expression of full-length or truncated forms of MN1. Expression profiles of MN1-induced leukemias arising from whole bone marrow transduction were also compared with the profiles obtained from the CMP cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE38767 | GEO | 2013/06/13

SECONDARY ACCESSION(S): PRJNA168600

REPOSITORIES: GEO

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Gene expression profiles in mouse common myeloid progenitor (CMP) and leukemia cells expressing full-length MN1 or truncated versions of MN1 protein

Project description:We used Affymetrix microarrays to characterize gene expression profiles that were perturbed in common myeloid progenitor (CMP) cells due to enforced expression of full-length or truncated forms of MN1. Expression profiles of MN1-induced leukemias arising from whole bone marrow transduction were also compared with the profiles obtained from the CMP cells. Lineage negative mouse bone marrow cells were transduced with retroviral vectors expressing full-length or truncated MN1 proteins. After 2 days in culture, cells were FACS-sorted for GFP expression and cultured for a further 3 days in growth media. After 5 days total, RNA was isolated and processed for microarray analysis. RNA was also prepared for microarray analysis from leukemias arising in mice following whole bone marrow transduction with full-lenght MN1.

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Project description:The molecular mechanism defining susceptibility of normal cells to oncogenic transformation may be a valuable therapeutic target. We characterized the cell of origin and its critical pathways in MN1 leukemias. Common myeloid (CMP), but not granulocyte-macrophage progenitors (CMP) could be transformed by constitutively overexpressed MN1. Complementation studies of CMP-signature genes in GMPs demonstrated that leukemogenicity of MN1 required the MEIS1/abdB-like HOX protein complex. Colocalization studies by ChIP-seq identified common chromatin targets of MN1 and MEIS1 that were associated with open chromatin and transcriptional activation. Transcriptional repression of MEIS1 target sites in established MN1 leukemias had antileukemic activity. As MN1 relies on but can not activate expression of MEIS1/abdB-like HOX proteins, transcriptional activity of these genes determines which cell is the cell of origin in MN1 leukemia. We have showed at the single cell level that CMPs, but not GMPs, are susceptible to MN1-induced transformation. To identify transcriptional differences between CMPs and GMPs that may explain this difference in susceptibilities to MN1 transformation we produced gene expression profiles (two biological replicates in each experimental arm) of bone marrow cells from MN1 leukemic mice and mature myeloid bone marrow cells (Gr1+/CD11b+) from healthy mice and compared those to already published gene expression profiles of CMPs and GMPs (Krivtsov, A.V., et al. (2006). Transformation from committed progenitor to leukaemia stem cell initiated by MLL-AF9. Nature 442, 818-822).

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Project description:Gene expression profiles in mouse common myeloid progenitor (CMP) and leukemia cells expressing full-length MN1 or truncated versions of MN1 protein

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