SDF-2 is involved in oxaliplatin resistance by maintaining ER homeostasis
| Project/Area Number |
17K15757
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Applied pharmacology
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| Research Institution | Waseda University |
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Principal Investigator |
Tanaka Masako 早稲田大学, 高等研究所, 講師(任期付) (00733651)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2018: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2017: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 抗がん剤耐性 / オキサリプラチン / カルシウム恒常性 / 胃がん細胞株 / 小胞体ストレス応答 / 胃がん / ストレス応答 |
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| Outline of Final Research Achievements |
We identified SDF-2 as a novel factor in oxaliplatin resistance; however, the molecular mechanisms of SDF-2-mediated resistance have remained unknown. This study aimed to investigate the molecular function of SDF-2 in the ER of cancer cells. We used SDF-2 knockout cells to analyze how they affect ER functions, including unfolded protein response, protein glycosylation, and Ca2+ homeostasis. As a result, we found that SDF-2 is involved in cell growth and oxaliplatin resistance by maintaining ER Ca2+ homeostasis.
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| Academic Significance and Societal Importance of the Research Achievements |
抗がん剤の耐性は薬剤そのものに対する抵抗性と細胞死に対する抵抗性に大別される。小胞体機能としては、小胞体ストレス応答の亢進が細胞死を抑制し、抗がん剤耐性を生じさせることが知られていたが、Ca2+の恒常性維持も細胞死の抑制に寄与する可能性を見出した。オキサリプラチンを含め抗がん剤の耐性を解除する治療薬はなく、奏効する既存薬を再び使用できるようになる耐性解除薬の開発に繋がる重要な知見を得た。
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Report
(4 results)
Research Products
(14 results)
