| Project/Area Number |
18K16270
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 55010:General surgery and pediatric surgery-related
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| Research Institution | Osaka Medical and Pharmaceutical University |
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Principal Investigator |
Fujioka Hiroya 大阪医科薬科大学, 医学部, 非常勤講師 (50773719)
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| Project Period (FY) |
2018-04-01 – 2024-03-31
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| Project Status |
Completed (Fiscal Year 2023)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2020: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2019: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2018: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
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| Keywords | パクリタキセル耐性 / 乳癌 / Stathmin / パクリタキセル耐性株 / 乳癌細胞株 / プロテオーム解析 / PKM / ホルモン耐性 / 薬剤耐性 / パクリタキセル |
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| Outline of Final Research Achievements |
In this study, an improved proteome analysis was performed using the breast cancer cell line MCF-7 (parental line) and paclitaxel (PTX). As a result, several proteins were identified compared to the parental cell line. In particular, the expression of Stathmin protein, which is involved in mitosis and associated with disease progression, and Pyruvate kinase M1/M2 (PKM1/PKM2), enzymes related to glucose metabolism, were upregulated in the resistant strain, as were PKM1 and PKM2 This result is consistent with the results of the previous study. These results suggest that sugar metabolism is enhanced in cancer cells during the acquisition of resistance.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究からStathminやPKM1の発現が抗癌剤耐性と関連していることを示すことにより、これらのタンパク質をターゲットとした新規治療薬の開発が期待される。またStathminやPKM1、また特定のmicroRNAの発現変化を診断・予後マーカーとして利用することで、早期の耐性発現を予測し、治療方針を迅速に変更することが可能となる。これにより、患者個々に最適化された治療を提供するための基盤が築かれる。
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