Analysis of negative transcription mechanism via ER and AR activated by shared ligands in breast and prostate cancers.
| Project/Area Number |
25870750
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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 molecular and cellular biology
Tumor therapeutics
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| Research Institution | Teikyo University |
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Principal Investigator |
SUSA TAKAO 帝京大学, 医学部, 助教 (20445852)
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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 |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 前立腺癌 / LNCaP / エストロゲン / アンドロゲン / AR / PTHrP / 核内受容体 / ER / MCF7 / ステロイドホルモン / 性ステロイドホルモン |
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| Outline of Final Research Achievements |
Most prostate cancers rely largely on the androgen-androgen receptor (AR) axis. In this study, we demonstrated the physiological signaling pathway between wild-type of AR and E2 in LNCaP cells, while the mutated AR (Thr-Ala877) expressed in the LNCaP cells has been reported to partially lose its ligand specificity and cross-react with several steroid hormones including E2. We speculate the existence of unknown regulatory mechanistic links between the AR signaling axis and E2 in LNCaP cells and other sex hormone-responsive cancer cells, and revealing these will be a novel finding. It is desirable to develop drugs targeting such cell-type-specific crosstalk between sex hormones with the ability to overcome anti-hormone resistance in certain types of prostate cancers.
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Report
(4 results)
Research Products
(21 results)
