2020 Fiscal Year Final Research Report
Study of insulin signal activation by TIGAR in colorectal cancer microenvironment
Project/Area Number |
18K08634
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Review Section |
Basic Section 55020:Digestive surgery-related
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Research Institution | Kawasaki Medical School |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
永坂 岳司 川崎医科大学, 医学部, 准教授 (30452569)
眞部 紀明 川崎医科大学, 医学部, 教授 (50403572)
上野 富雄 川崎医科大学, 医学部, 教授 (70284255)
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Project Period (FY) |
2018-04-01 – 2021-03-31
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Keywords | 大腸癌 / TIGAR / インスリン抵抗性 |
Outline of Final Research Achievements |
TIGAR gene promoter methylation analysis using colorectal cancer clinical specimens demonstrated that there were no significant differences between methylated and unmethylated group about neither relapse free survival (RFS) or overall survival (OS). There was tendency that methylated group had better OS. Moreover, there were no significant differences between TIGAR protein expression and RFS or OS, but there was tendency that worse RFS was shown in the group of high expression of TIGAR. This study could demonstrate some definite relation between TIGAR and colorectal cancer, but could not elucidate unexplained parts of mechanism of carcinogenesis by TIGAR activation.
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Free Research Field |
消化器外科学
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Academic Significance and Societal Importance of the Research Achievements |
p53の下流に位置するTIGARの活性化は糖新生を亢進し、そのノックアウトマウスでは腫瘍増殖能が減少する。本研究においてTIGARは大腸癌において有意にメチルされる遺伝子の一つの可能性であることが分かった。ただ我々の限定的な研究においてはメチル化群と長期予後との明らかな因果関係を認めることは出来なかった。またTIGARタンパク高発現群は再発が起こりやすい傾向にあった。今後TIGAR活性による発がん機構を解明することによりTIGAR標的新規創薬・治療の開発に向けたさらなる基礎研究と今後の臨床応用への礎を構築できると考える。
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