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2023 Fiscal Year Final Research Report

Recognition of non-canonical MHC-I by epithleial cells and elimination of transformed cells

Research Project

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Project/Area Number 21K07107
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Review Section Basic Section 50010:Tumor biology-related
Research InstitutionWaseda University

Principal Investigator

Kamoshita Nagisa  早稲田大学, 理工学術院, 研究助手 (30835814)

Project Period (FY) 2021-04-01 – 2024-03-31
Keywords発がん制御 / 超早期がん
Outline of Final Research Achievements

It has been found that stimulated MHC-Ib expressed on epithelial cells induces cell death through the reverse signaling. Identification of candidate ligand molecules for MHC-Ib, which is essential for elucidating the reverse signaling mechanism, and analysis of the cell death induction mechanism via MHC-Ib were conducted. The minimal peptide of the identified ligand binding with MHC-I induced cell death in vitro. Additionally, MHC-Ib stimulated by the minimal peptide activated the MAPK pathway. This revealed that the induced cell death is through Apoptosis mediated by Caspase3 activation. Furthermore, application of the peptide in mouse in vivo experiments resulted in suppression of carcinogenesis.

Free Research Field

腫瘍生物学

Academic Significance and Societal Importance of the Research Achievements

本研究では、がん変異細胞の排除を抑制する機構を解明した。このMHC-Ibによる抑制機構を解除することで、MHC-Ia/AltRによる変異細胞の排除シグナルをより効率的に促進でき、予防するための治療法確立に繋がる。本研究で解明される抑制機構を解除することは、まさにこのがん変異細胞の排除を促進するために有効な手段である。そのため、予防的にがん変異細胞を排除する医療の確立に大きく貢献する。

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Published: 2025-01-30  

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