The role of nuclear actin filaments in cancer cells
Project/Area Number |
18K06231
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Review Section |
Basic Section 44010:Cell biology-related
|
Research Institution | Konan University |
Principal Investigator |
KAWAUCHI KEIKO 甲南大学, フロンティアサイエンス学部, 准教授 (40434138)
|
Co-Investigator(Kenkyū-buntansha) |
岩根 敦子 国立研究開発法人理化学研究所, 生命機能科学研究センター, チームリーダー (30252638)
|
Project Period (FY) |
2018-04-01 – 2023-03-31
|
Project Status |
Completed (Fiscal Year 2022)
|
Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2020: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2019: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2018: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
Keywords | がん / p53 / アクチン / 抗がん剤 / DNA損傷 / 核 / p53 / メカニカルストレス |
Outline of Final Research Achievements |
Actin remodeling is associated with not only cell migration but also cell survival and proliferation. Tumor suppressor p53 modulates actin dynamics in the cytoplasm upon stress-induced DNA damage; however, the role of p53 in the alteration of actin dynamics in the nucleus remains elusive. We found that p53 depletion promotes the formation of nuclear actin filaments when subjected to DNA-damaging agents. In addition, we identified the peptide that, upon treatment with a DNA-damaging agent, promoted nuclear actin filaments bundling in p53-depleted cells.
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Academic Significance and Societal Importance of the Research Achievements |
p53 機能の喪失は、悪性度高いがんで高頻度にみられ、治療抵抗性の一因となっている。p53機能の喪失が及ぼす抗がん剤処理による核アクチン線維の形成の促進効果を明らかにした本研究成果は、がんの薬剤耐性機構への理解が大きく深化し、学術的にもインパクトが高い。さらに、p53機能欠損細胞特異的に核アクチンファイバーの形成を誘導するペプチドを特定したことは、化学療法の効果を高める革新的ながん治療法の開発につながる。
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Report
(6 results)
Research Products
(17 results)