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2023 Fiscal Year Final Research Report

The PARP and ROS signaling pathways in the mechanism of action of anticancer drugs.

Research Project

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Project/Area Number 20K07210
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Review Section Basic Section 47060:Clinical pharmacy-related
Research InstitutionKinjo Gakuin University

Principal Investigator

Mizutani Hideki  金城学院大学, 薬学部, 教授 (80397504)

Project Period (FY) 2020-04-01 – 2024-03-31
Keywords抗がん薬 / PARP阻害薬
Outline of Final Research Achievements

PARP and ROS signalling mechanisms in the mechanism of action of anticancer drugs were investigated. The function of PARP was assessed with and without PARP inhibitors (e.g. olaparib). H2O2 (reaction time: 4 h) induced apoptosis and reduced cell viability in HL-60 cells. Pirarubicin (THP) (4 h) reduced cell viability in HL-60 cells and this reduction was not affected by olaparib. In contrast, THP (24 h) reduced cell viability against HL-60 cells, which was inhibited by olaparib. Doxorubicin (DOX) (24 h) reduced cell viability against HL-60 cells, which was enhanced by olaparib. This reduction was potentiated by olaparib.

Free Research Field

医療系薬学

Academic Significance and Societal Importance of the Research Achievements

抗がん薬の作用機序におけるPARPと活性酸素(ROS)シグナル伝達機構について検討することにより、抗がん薬の作用機序におけるPARPの働きを明らかにした。PARP, ROS,および関連する分子が抗がん薬治療の新しいバイオマーカーに成り得ることを示唆しており、新しいがん治療標的分子の提案につながり、これらを用いた新しいがん化学療法の開発と創薬への基盤情報となり得る。

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Published: 2025-01-30  

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