Effects of stress hormone on hormone metabolism and cancer growth in endometrial cancer

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K08338
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Human pathology
• Research Institution: Tohoku University
• Principal Investigator: Miki Yasuhiro 東北大学, 災害科学国際研究所, 講師 (50451521)
• Co-Investigator(Renkei-kenkyūsha): ITO Kiyoshi 東北大学, 災害科学国際研究所, 教授 (70241594) ; TAKAGI Kiyoshi 東北大学, 医学系研究科, 講師 (80595562)
• Research Collaborator: YOSHIDA Rena ; FUE Misaki
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 子宮内膜癌 / コルチゾール / アロマターゼ / グルココルチコイド受容体 / DHEA

Outline of Final Research Achievements

Intratumoral cortisol concentration was considered to be regulated by 11β-hydroxysteroid dehydrogenase (HSD) 1 and 11β-HSD2 in endometrial cancer. In endometrial cancer, cortisol induced enzymatic activity of estrogen synthase (aromatase) through glucocorticoid receptor (GR) located in the stromal cells but nor carcinoma cells. This finding suggests that cortisol contributed estrogen-dependency of endometrial cancer cells. It is also suggested that cortisol directly relates to cell growth through the induction of annexin A1 expression, which is known as a GR target gene, in stromal cells of endometrial cancer. Dhydroepiandrosterone (DHEA), which is also known as a stress-related hormone, was synthesized by steroid sulfatase in endometrial cancer tissue.

Free Research Field

腫瘍学　内分泌学