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2022 Fiscal Year Final Research Report

Comprehensive epigenomic analysis to identify AR-V7 target genes in prostate cancer

Research Project

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Project/Area Number 20K09572
Research Category

Grant-in-Aid for Scientific Research (C)

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

Principal Investigator

Imamura Yusuke  千葉大学, 医学部附属病院, 講師 (10568629)

Co-Investigator(Kenkyū-buntansha) 坂本 信一  千葉大学, 医学部附属病院, 准教授 (70422235)
Project Period (FY) 2020-04-01 – 2023-03-31
Keywords前立腺癌
Outline of Final Research Achievements

One of the molecular mechanisms leading to CRPC is the aberrant expression of Splicing Variants, specifically Androgen Receptor Splicing Variant 7 (AR-V7), in which the ligand-binding site of the androgen receptor (AR) is deleted. To elucidate the target gene of AR-V7 and to develop a new therapeutic strategy for CRPC, we have performed RNA-seq and ChIP-seq using a next-generation sequencer. We performed integrated analysis of gene expression, AR binding sites, AR-V7 binding sites, and histone modification changes by RNA-seq and ChIP-seq using next-generation sequencers to comprehensively identify downstream target genes of AR-V7 and their regulation, and to analyze the function of downstream target genes.

Free Research Field

泌尿器悪性腫瘍

Academic Significance and Societal Importance of the Research Achievements

去勢抵抗性前立腺癌におけるAR-V7発現は、AR増幅などとならびホルモン抵抗性の重要な機序の1つであるが、ARと共通する下流標的、ARとは異なる独自の下流標的など詳細な解明がなされておらず、その標的治療が未開発である。CRPCに対する新規ホルモン治療薬や抗がん剤治療薬が現在、臨床応用されているが、新たな治療抵抗性の獲得や副作用がしばしば問題となり、新たな治療戦略の確立が急務である。AR-V7の結合領域や周辺のエピゲノム変化、発現変化の統合的かつ網羅的解析によりこれまでとは全く異なる新たな治療戦略につながる可能性を有していたと考えられる。

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Published: 2024-01-30  

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