2021 Fiscal Year Final Research Report

The regulation of cancer recurrence by the construction of immunosurveilance targeing cell cycle withdrawal/reentry cancer cell

Research Project

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Project/Area Number	19K22662
Research Category	Grant-in-Aid for Challenging Research (Exploratory)
Allocation Type	Multi-year Fund
Review Section	Medium-sized Section 55:Surgery of the organs maintaining homeostasis and related fields
Research Institution	Kyushu University
Principal Investigator	ONISHI Hideya 九州大学, 医学研究院, 准教授 (30553276)
Co-Investigator(Kenkyū-buntansha)	中村雅史九州大学, 医学研究院, 教授 (30372741) 三好圭九州大学, 大学病院, 助教 (70755272) 山崎章生九州大学, 医学研究院, 共同研究員 (80404440) 永井俊太郎九州大学, 大学病院, 助教 (90755240)
Project Period (FY)	2019-06-28 – 2022-03-31
Keywords	細胞周期離脱癌 / 細胞周期再進入癌 / 免疫監視機構構築 / G0/G1アレスト / 癌休眠 / Hedgehog signal / PTPN3 / C4orf47
Outline of Final Research Achievements	The comprehensive analysis of the cell cycle withdrawal/reentry cancer cell inducing gene was performed and 3 genes were identified. GLI2 was involved with cyclinD1 expression. PTPN3 contributed to the phosphorylation of tyrosine kinase by the upregulation of CACNA1G expression that is calcium ion channel. C4orf47 contributed to the cell dormancy through G0/G1 arrest.
Free Research Field	臨床腫瘍学
Academic Significance and Societal Importance of the Research Achievements	GLI2遺伝子がcyclinD1発現に関与すること、PTPN3がカルシウムチャネルCACNA1G発現を介してチロシンキナーゼリン酸化に関与すること、およびC4orf47がG0/G1アレストに関与し細胞休眠に関与することを新たに見出した。この3遺伝子は細胞周期離脱癌(G0癌)/細胞周期再進入癌の誘導遺伝子と考えられ、癌再発制御への研究の足掛かりになると考える。