Molecular analysis of tumor suppressor gene NDRG2 function and regulation of expression
| Project/Area Number |
25860242
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Pathological medical chemistry
|
|---|
| Research Institution | University of Miyazaki |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2013-04-01 – 2015-03-31
|
| Project Status |
Completed (Fiscal Year 2014)
|
| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
|---|
| Keywords | 癌 / シグナル伝達 / ストレス / 成人病 |
|---|
| Outline of Final Research Achievements |
We reported that novel tumor suppressor gene NDRG2 (N-myc downstream-regulated gene 2) regulate signal transduction of PI3K/AKT and NF-kappaB (NFκB) pathway through the suppression of PTEN phosphorylation, resulting in the involvement of tumorigenesis. We demonstrated that transient stress response including inflammation induces NDRG2 expression via NFκB pathway. Therefore, the transient stress-induced signal transduction is negatively feedback regulated by NFκB-induced NDRG2 expression. Furthermore, chronic stress promotes the own-regulation of NDRG2 through DNA promoter methylation. These finding suggest that elucidating the mechanism of NDRG2 function and regulation of expression may become a new therapeutic target for many type of disease.
|
Report
(3 results)
Research Products
(10 results)
-
[Journal Article] Loss of NDRG2 expression activates PI3K-AKT signalling via PTEN phosphorylation in ATLL and other cancers.2014
Author(s)
Nakahata S, Ichikawa T, Maneesaay P, Saito Y, Nagai K, Tamura T, Manachai N, Yamakawa N, Hamasaki M, Kitabayashi I, Arai Y, Kanai Y, Taki T, Abe T, Kiyonari H, Shimoda K, Ohshima K, Horii A, Shima H, Taniwaki M, Yamaguchi R, Morishita K.
-
Journal Title
Nat Commun
Volume: in press
Issue: 1
Pages: 3393-3393
DOI
Related Report
Peer Reviewed / Open Access
-
-
-
-
-
-
-
-
-
