Analysis of an epigenetic switch leading to estrogen-independent cell proliferation

2016 Fiscal Year Final Research Report

• Project/Area Number: 26340038
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Risk sciences of radiation and chemicals
• Research Institution: Osaka University
• Principal Investigator: Wada Tadashi 大阪大学, 工学研究科, 特任教授(常勤) (60262309)
• Co-Investigator(Renkei-kenkyūsha): WATANABE Hajime 大阪大学, 大学院工学研究科, 教授 (80212322) ; ONEYAMA Chitose 愛知県がんセンター研究所, 感染腫瘍学部, 部長 (90373208)
• Research Collaborator: KITAMURA Ayaka ; TAKATA Ryouhei ; MAKADO Goki
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: エストロゲン / 膣 / DES / 女性ホルモン / 遺伝子 / 転写

Outline of Final Research Achievements

Neonatal exposure of DES induced persistent hyperplasia of epithelial cells in the vagina of mice. In this study, we showed that inflammatory transcription factor is likely to be activated by neonatally DES exposure, suggesting that DES-dependent hyperplasia may be associated with inflammatory reactions. In addition, CAGE (Cap Analysis of Gene Expression) analysis revealed that increased expression of certain non-coding RNAs was observed by the DES-exposure at the neonatal stage of mice.

Free Research Field

分子生物学