2016 Fiscal Year Final Research Report
Analysis on promoted ubiquitination of estrogen receptor by histone acetyltransferase Hbo1
Project/Area Number |
26460400
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Pathological medical chemistry
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Research Institution | Teikyo University |
Principal Investigator |
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Project Period (FY) |
2014-04-01 – 2017-03-31
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Keywords | ユビキチン化 / エストロゲン受容体 |
Outline of Final Research Achievements |
Approximately two thirds of breast cancers grow in an estrogen-dependent fashion. Hormonal therapy, which inhibits estrogen action, has been proven effective in treatment of those breast cancers. However, resistance to such therapies often arises, complicating treatment of breast cancer patients. Estrogen signal for proliferation is transmitted into cell via estrogen receptor. Thus, it is of importance to understand fully molecular mechanism of how estrogen receptor is produced, degraded, or transferred within the cell. I have found a novel mechanism of how estrogen receptor protein is degraded: histone acetyltransferase Hbo1, involved in DNA replication, ubiquitinates estrogen receptor directly and stimulates ubiquitin-dependent proteasomal degradation. This degradation of estrogen receptor appears to contribute to cycled DNA binding and proteolysis of estrogen receptor, leading to continued activation of estrogen-dependent transcription.
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Free Research Field |
生化学 分子腫瘍学 クロマチン
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