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2018 Fiscal Year Final Research Report

The clarification of a tumorigenesis of malignant rhabdoid tumor through a understanding of control mechanism of RUNX1 by hSNF5

Research Project

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Project/Area Number 16K10038
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Pediatrics
Research InstitutionKyoto Prefectural University of Medicine

Principal Investigator

Kuwahara Yasumichi  京都府立医科大学, 医学(系)研究科(研究院), 講師 (30590327)

Co-Investigator(Kenkyū-buntansha) 奥田 司  京都府立医科大学, 医学(系)研究科(研究院), 教授 (30291587)
Project Period (FY) 2016-04-01 – 2019-03-31
KeywordsRUNX1 / SWI/SNF複合体 / 悪性ラブドイド腫瘍
Outline of Final Research Achievements

To elucidate alterations of functions of transcription factor with a loss of SNF5, we focused the relationship between SWI/SNF complex and transcription factor, RUNX1 on p21 locus in malignant rhabdoid tumor (MRT) cells. We indicated that RUNX1 binds to SWI/SNF complex with or without SNF5 via C-terminal of RUNX1. A loss of SNF5 caused an increase of RUNX1 recruitment on p21 promoter region, followed by an aberrant of transcription activities of p21 gene.
SWI/SNF complex interacts with transcription factor to regulate transcription activities. However, SWI/SNF complex without SNF5 has abnormal function to transcription factors, resulted in abnormal control of gene expressions.

Free Research Field

転写機構、小児がん

Academic Significance and Societal Importance of the Research Achievements

MRTは乳幼児に発症する予後の悪い小児固形腫瘍である。SNF5遺伝子の単一の異常でMRTは発症するため、病態の解明や治療法の開発にはSNF5遺伝子の機能解析は重要であるものの、十分解明されてはいない。また、SNF5と関係性のある転写因子を解析した研究の報告は少なく限定的であった。今回、SNF5欠損による転写因子との相互作用の変更が確認されたが、今後SNF5欠損によって影響している転写因子の解明が、有効な治療法の開発に直結することが示された点で意義のある研究結果である。

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Published: 2020-03-30  

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