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The role of microRNA142 overexpression in B-cell tumor development

Research Project

Project/Area Number 25461433
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Hematology
Research InstitutionWakayama Medical University

Principal Investigator

SONOKI TAKASHI  和歌山県立医科大学, 医学部, 教授 (30382336)

Project Period (FY) 2013-04-01 – 2016-03-31
Project Status Completed (Fiscal Year 2015)
Budget Amount *help
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
KeywordsB細胞性腫瘍 / 染色体転座 / マイクロRNA / Bリンパ腫 / モデルマウス / B細胞性リンパ腫 / 分化阻害 / 発がん / microRNA
Outline of Final Research Achievements

(Summary) We performed functional analyses of miR142 using two mouse models. As a result, miR142 overexpression was found to cause a decrease in blood cells. (Result) (1) Bone marrow transplantation model: MiR142 and the GFP genes were introduced into bone marrow cells. The genes-introduced bone marrow cells were transplanted into the bone marrow-disrupted mouse. As a result, the blood cells which strongly express the miR142 were reduced. (2) Genetically modified model: Genetically modified mouse to be strongly expressed in B cells was generated. In genetically modified mice that were older than one year of age, IgM-positive cells were reduced compared to the wild type. (Conclusion) As mentioned above, our results suggest that miR142 overexpression is involved in the cancer development through disruption of cell fate.

Report

(4 results)
  • 2015 Annual Research Report   Final Research Report ( PDF )
  • 2014 Research-status Report
  • 2013 Research-status Report

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Published: 2014-07-25   Modified: 2019-07-29  

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