Analysis of negative transcription mechanism via ER and AR activated by shared ligands in breast and prostate cancers.

2015 Fiscal Year Final Research Report

• Project/Area Number: 25870750
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Applied molecular and cellular biology; Tumor therapeutics
• Research Institution: Teikyo University
• Principal Investigator: SUSA TAKAO 帝京大学, 医学部, 助教 (20445852)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 前立腺癌 / LNCaP / エストロゲン / アンドロゲン

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.

Free Research Field

分子生物学