Molecular mechanism of estrogen supply pathway in hormone-sensitive breast cancer
Project/Area Number |
16K18951
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Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Multi-year Fund |
Research Field |
Medical pharmacy
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Research Institution | Nagoya City University |
Principal Investigator |
Yasujima Tomoya 名古屋市立大学, 大学院薬学研究科, 講師 (50753555)
|
Project Period (FY) |
2016-04-01 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
|
Keywords | トランスポーター / エストロゲン / 乳がん / 小胞体 / エストロゲン硫酸 / 促進拡散 / がん / 癌 |
Outline of Final Research Achievements |
Sulfate-conjugated estrogens were transported into cells by various organic anion transporters localized on the cell membrane. Since sulfate-conjugated estrogen itself cannot bind to estrogen receptor, sulfate conjugation is removed by steroid sulfatase (STS) in the cell. However, since STS has an active site inside the endoplasmic reticulum membrane, it is necessary to transport sulfate conjugate into the endoplasmic reticulum to exert its physiological activity. We succeeded in identifying the steroid sulfate transporter 1 (SST1) which plays a role in regulating estrogen concentration. It was found that thyroid hormones inhibited the function of SST1, they possibly control the function of SST1.
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Report
(3 results)
Research Products
(4 results)