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Mouse Models of Cancer Study02:43

Mouse Models of Cancer Study

Mice have long served as models for studying human biology and pathology because of their phylogenetic and physiological similarity with humans. They are also easy to maintain and breed in the laboratory, and hence, many inbred strains are now available for research. Studies on mice have contributed immeasurably to our understanding of cancer biology.
The development of transgenic, knockout, and knock-in mice has led to an exponential increase in their use as model organisms in research,...

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Eμ/miR-125b transgenic mice develop lethal B-cell malignancies.

Y Enomoto1, J Kitaura, K Hatakeyama

  • 1Division of Cellular Therapy, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.

Leukemia
|July 9, 2011
PubMed
Summary
This summary is machine-generated.

MicroRNA-125b-1 (miR-125b-1) overexpression drives B-cell malignancies in a mouse model. This study reveals miR-125b-1 as a key factor in precursor B-cell tumor development and identifies Trp53inp1 as a novel target.

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Area of Science:

  • Hematology
  • Molecular Biology
  • Oncology

Background:

  • MicroRNA-125b-1 (miR-125b-1) is frequently overexpressed in B-cell precursor acute lymphoblastic leukemia (BCP-ALL), often due to the t(11;14) translocation.
  • Overexpression of miR-125b-1 is also observed in BCP-ALL patients lacking the t(11;14) translocation, as well as in BCR/ABL-positive BCP-ALL and chronic myelogenous leukemia-derived B-cell lymphoid crisis.

Purpose of the Study:

  • To investigate the role of deregulated miR-125b-1 expression in the in vivo development of B-cell tumors.
  • To elucidate the molecular mechanisms by which miR-125b-1 contributes to B-cell tumorigenesis.

Main Methods:

  • Generation of Emicro/miR-125b-TG transgenic mice that overexpress miR-125b-1 under the control of immunoglobulin heavy chain (IGH) regulatory elements, mimicking the t(11;14) translocation.
  • In vitro and in vivo analysis of B-cell malignancies, apoptosis resistance, and gene targeting in Emicro/miR-125b-TG mice.
  • Identification of novel miR-125b-1 target genes in hematopoietic cells.

Main Results:

  • Emicro/miR-125b-TG mice developed lethal B-cell malignancies, both IgM-negative and IgM-positive, characterized by clonal proliferation.
  • B cells from these mice exhibited resistance to serum starvation-induced apoptosis.
  • Trp53inp1, a pro-apoptotic gene, was identified as a novel in vitro and in vivo target of miR-125b-1 in hematopoietic cells.

Conclusions:

  • miR-125b-1 plays a significant role in the tumorigenesis of precursor B cells.
  • The overexpression of miR-125b-1 contributes to B-cell malignancy development by promoting apoptosis resistance and potentially through targeting genes like Trp53inp1.