| Project/Area Number |
15K19303
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Gastroenterology
|
|---|
| Research Institution | Asahikawa Medical College |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2015-04-01 – 2018-03-31
|
| Project Status |
Completed (Fiscal Year 2017)
|
| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
|---|
| Keywords | 膵癌 / 長鎖機能性RNA / 細胞外小胞 / 上皮間葉形質転換 / long non-coding RNA / extracellular vesicles / EMT / microRNA / Long non-coding RNA / Extracellular vesicle |
|---|
| Outline of Final Research Achievements |
TGF-b induced epithelial-mesenchymal transition (EMT) is a trigger of invasion and metastasis in pancreatic cancer (PDAC). De-regulated expression of long non-coding RNAs (lncRNAs) has been reported to be correlated with several diseases. However, their roles to EMT in PDAC remain unclear. Some lncRNAs are transferred by extracellular vesicles (EVs). Although EV-encapsulated ncRNAs have been reported to serve as biomarkers for cancers, there is only a handful information regarding “EV lncRNA”.
We investigated EV mediated transfer of lncRNA in PDAC. We identified lncRNA HULC is increased in PDAC cells and their EVs. HULC could promote cell invasion and migration via induction of EMT through transfer by EVs. Moreover, miR-133b could target HULC and attenuate cell invasion and migration via suppression of EMT. Furthermore, EV encapsulated HULC derived from PDAC patient serum would be a useful biomarker for human PDAC.
|
