Molecular mechanism of solid tumor growth inhibition by a new differentiation inducer and molecular target agents
| Project/Area Number |
25462007
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
General surgery
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| Research Institution | Shimane University (2014-2015)
Research Institute for Clinical Oncology, Saitama Cancer Center (2013) |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | コチレニンＡ / 三酸化ヒ素 / 分化誘導剤 / 乳癌細胞 / 増殖抑制 / 併用効果 / アポトーシス / 活性化酸素 / 癌 / 薬剤反応性 / シグナル伝達 / フェロトーシス / 発生・分化 / 薬剤反応 |
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| Outline of Final Research Achievements |
We have examined whether a new differentiation inducer of leukemia cells can suppress the proliferation of solid tumor cells. In this study we found that cotylenin A significantly potentiate arsenic trioxide-induced inhibition of cell growth of human breast and pancreatic cancer cells. The combined treatment with cotylenin A and arsenic trioxide induced cleaved caspase-7 in human breast cancer MCF-7 cells at the concentration which arsenic trioxide alone scarcely induced and cotylenin A alone only weakly induced. Expression of survivin was markedly decreased with the presence of both cotylenin A and arsenic trioxide. The pretreatment with N-acetylcysteine significantly reduced the combination treatment-induced cell growth inhibition. These data suggest that induction of cleaved caspase-7, inhibition of survivin and oxidative responses are important events in the corporative inhibition in the growth of MCF-7 cells.
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Report
(4 results)
Research Products
(7 results)
