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2022 Fiscal Year Final Research Report

Significance of MUC1 and chromatin remodeling factor complexes in neuroendocrine prostate cancer

Research Project

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Project/Area Number 20K09568
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Review Section Basic Section 56030:Urology-related
Research InstitutionKeio University

Principal Investigator

Yasumizu Yota  慶應義塾大学, 医学部(信濃町), 助教 (40464854)

Co-Investigator(Kenkyū-buntansha) 小坂 威雄  慶應義塾大学, 医学部(信濃町), 講師 (30445407)
Project Period (FY) 2020-04-01 – 2023-03-31
Keywords神経内分泌前立腺癌 / SWI/SNF / BRG1 / ARID1A
Outline of Final Research Achievements

We investigated the role of MUC1 and mSWI/SNF in castration-resistant prostate cancer. We found that MUC regulates the expression of BRG1 and ARID1A, which constitute mSWI/SNF through the transcription factor E2F1. Furthermore, we found that MUC1 regulates the expression of BRG1 and ARID1A in the transcription regulatory regions of NOTCH1 and NANOG through E2F1 and acquires self-renewal ability. These results suggested that the MUC1-E2F1-mSWI/SNF-NOTCH1-NANOG pathway is involved in stem cell acquisition of prostate cancer.

Free Research Field

神経内分泌前立腺癌

Academic Significance and Societal Importance of the Research Achievements

神経内分泌前立腺癌(NEPC)への脱分化にTP53やRB1といった癌抑制遺伝子の変異が関与する。そして2nd stepとして転写・翻訳の調整スイッチが入ることで神経内分泌分化が生じる。この転写・翻訳の調整のことをエピジェネティックリプログラミングと呼ぶ。今回、我々はMUC1がSWI/SNFに作用することで、NEPC分化の調整スイッチを担っていることを世界に先駆けて発見した。NEPCは難治性でいまだ治療方法が確立していない。本研究の結果は未知なるNEPCの分子基盤を解明し、NEPCの新規治療戦略確立の一助となる。

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Published: 2024-01-30  

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