Basic and clinical research toward the development of treatment with HDAC inhibitors for breast cancer
| Project/Area Number |
22591425
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General surgery
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| Research Institution | Kanazawa University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
OHTA Tetsuo 金沢大学, 医学系, 教授 (40194170)
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| Project Period (FY) |
2010-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2013: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2010: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
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| Keywords | 乳腺外科学 / エピジェネティックス |
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| Research Abstract |
We focused on valproic acid (VPA), an anticonvulsant drug, which has been reported as histone deacetylase (HDAC) inhibitor, and researched for the new therapeutic development of breast cancer using VPA. We confirmed VPA suppressed the proliferation of breast cancer cell lines in each subtypes in the concentrations equivalent to those used for the clinical treatment in concentration-dependent to varying degrees. We also confirmed VPA induced breast cancer cells to differentiation and apoptosis. We showed the anti-proliferative mechanism of VPA might be associated with not only the direct function of acetylation of histone, through cell cycle arrest or apoptosis, but also indirect function that that acetylation of HSP70 disrupted the function of HSP90 and led to down-regulation of its client proteins such as HER2.
This study suggests combination of standard treatment for breast cancer and VPA can be useful in terms of proliferative suppression of cancer in the future.
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Report
(5 results)
Research Products
(2 results)
