Transcriptomics

Dataset Information

3

Musashi 2 regulates normal hematopoiesis and accelerates leukemogenesis (LK and MS12-inducible)


ABSTRACT: We demonstrate that Msi2 is the predominant form expressed in hematopoietic stem cells (HSC), and its knockdown leads to reduced engraftment and depletion of HSCs in vivo. Overexpression of Msi2 in a mouse model increases HSC cell cycle progression and cooperates with BCR-ABL1 to induce an aggressive leukemia. MSI2 is over-expressed in human myeloid leukemia, and expression levels directly correlate with decreased patient survival, thereby defining MSI2 expression as a novel prognostic marker in acute myeloid leukemia (AML). Depletion of MSI2 in human myeloid leukemia cells leads to decreased proliferation and apoptosis. These data implicate the MSI2 RNA binding protein in myeloid leukemogenesis and identify a novel potential target for therapy in AML. Hematopoietic stem cells and progenitor cells (LineageLow, Sca1-, Kit+; LK) from control and transgenic MSI2-inducible mice were isolated and RNA was extracted using Qiagen RNeasy Micro Kit according to manufacturers instruction. cDNA was fragmented and biotinylated before hybridization onto Affymetrix Mouse Expression Array 430 2.0.

ORGANISM(S): Mus musculus  

SUBMITTER: Benjamin L Ebert   Rachel Okabe  D G Gilliland  Fatima Al-Shahrour  Stefan Fröhling  Maricel Gozo  Kelly Morgan  Steven W Lane  Lars Bullinger  Mahnaz Paktinat  Mark Fleming  Brian Ball  Christopher J Lengner  Winnie Tam  Claudia Scholl  Rudolf Jaenisch  Samir Zaidi  William Einhorn  George Q Daley  Michael G Kharas 

PROVIDER: E-GEOD-22773 | ArrayExpress | 2010-07-21

SECONDARY ACCESSION(S): GSE22773PRJNA129113

REPOSITORIES: GEO, ArrayExpress

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Publications


RNA-binding proteins of the Musashi (Msi) family are expressed in stem cell compartments and in aggressive tumors, but they have not yet been widely explored in the blood. Here we demonstrate that Msi2 is the predominant form expressed in hematopoietic stem cells (HSCs), and its knockdown leads to reduced engraftment and depletion of HSCs in vivo. Overexpression of human MSI2 in a mouse model increases HSC cell cycle progression and cooperates with the chronic myeloid leukemia-associated BCR-ABL  ...[more]

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