| Project/Area Number |
15K09432
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Endocrinology
|
|---|
| Research Institution | Kobe University |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
高橋 裕 神戸大学, 医学研究科, 准教授 (70301281)
|
|---|
| Co-Investigator(Renkei-kenkyūsha) |
YAMADA Shozo 虎の門病院, 間脳下垂体腫瘍外科 (80260131)
|
|---|
| Research Collaborator |
YOSHIDA Kenichi
|
|---|
| Project Period (FY) |
2015-04-01 – 2018-03-31
|
| Project Status |
Completed (Fiscal Year 2017)
|
| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
|
|---|
| Keywords | Cushing disease / long non-coding RNA / proliferation / invasiveness / ACTH / lncRNA / Cushing病 / 下垂体腺腫 / エピジェネティクス / 浸潤性 / miRNA / non-coding RNA / Lnc RNA / 内分泌腫瘍 / 細胞周期 / クッシング病 / 分子標的薬 |
|---|
| Outline of Final Research Achievements |
In this research, we explored long non-coding RNA (lncRNA) which associated with proliferation and invasiveness in ACTH producing pituitary adenoma (ACTHoma). First, we divided specimens of ACTHoma from 7 patients according to Knosp grade; grade <2, and grade 2 and more, and compared their lncRNA expression levels using microarray analysis. Furthermore, we measured RNA levels of 30 ACTHoma specimens and compared with their clinical characterization. Then we found lncRNA CRNDE, which expressed 3.6 fold in tumors with grade 2 and more.
CRNDE expressed 3 fold in macroadenoma than in microadenoma, suggesting this lncRNA is associated with tumor proliferation in addition to invasiveness. CRNDE located in cytoplasm of ACTHoma, indicating the mechanism related to proliferation and invasiveness by CRNDE is mediated via microRNA or mRNA stability as an epigenetic regulation. Further molecular mechanism needs to be analyzed of CRNDE in ACTHoma as a potential therapeutic target.
|
