2015 Fiscal Year Final Research Report
Mechanisms of colon cancer malignancy regulation by two endogenous prostanoid receptors
Project/Area Number |
25460091
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Pharmacology in pharmacy
|
Research Institution | Chiba University |
Principal Investigator |
FUJINO Hiromichi 千葉大学, 薬学研究科(研究院), 准教授 (40401004)
|
Co-Investigator(Renkei-kenkyūsha) |
MURAYAMA Toshihiko 千葉大学, 大学院薬学研究院, 教授 (90174317)
|
Project Period (FY) |
2013-04-01 – 2016-03-31
|
Keywords | Gタンパク質共役型受容体 / プロスタノイド / 細胞内情報伝達系 / バイアスリガンド |
Outline of Final Research Achievements |
Prostaglandin D2 (PGD2) and prostaglandin E2 (PGE2) are known as positional-isomers so that they are known to cross-talk to the other receptors besides its own cognate receptors. However, the physiological roles and/or significances of the cross-talks have been remained unclear. In this study, we have elucidated that PGD2 or PGE2 acts to DP receptors or EP2 receptors not as a partial agonist but as a biased ligand followed by activating a biased signaling pathway, respectively. It is widely reported that PGD2 has a role on anti-cancer activity whereas PGE2 has a pro-cancer activity. The findings about the biased activity evoked by endogenous prostanoids as biased agonists are very significant that may answer the reasons why both prostanoids show the opposite functions in the body. We believe that our study will provide innovated ideas and/or approaches in the field of understanding physiological functions of the G protein-coupled receptors including prostanoid receptors.
|
Free Research Field |
分子細胞薬理学
|