Establishment of newly treatment strategies for suppressing desmoplasitic reactions in pancreatic cancer
| Project/Area Number |
22790652
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Gastroenterology
|
|---|
| Research Institution | Kyushu University |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2010 – 2011
|
| Project Status |
Completed (Fiscal Year 2011)
|
| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2011: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2010: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
|---|
| Keywords | 胆道学 / 膵臓学 / 膵癌 / 間質細胞 |
|---|
| Research Abstract |
We investigated whether the antifibrotic agent, pirfenidone(PF), suppress desmoplasia and exert anti-tumor effects for pancreatic cancer. PF inhibited proliferation, invasiveness and migration of PSCs in the dose-dependent manner. The supernatants of PSCs treated with PF attenuated capacity to promote proliferation, invasiveness and migration of pancreatic cancer cells. The supernatants of pancreatic cancer cells increased production of PDGF-A, HGF, collagen type I, Fibronectin, and periostin in PSCs, and the increase were significantly reduced by PF. In vivo, PF significantly suppressed the tumor growth only when pancreatic cancer cells were co-transplanted with PSCs and decreased numbers of PSCs and deposition of collagen type I and periostin in tumors. Combination treatment with gemcitabine and PF more effectively suppressed in vivo tumor growth than gemcitabine alone and PF alone groups. These results indicate that PF could be promising agents targeting desmoplasia by suppression of PSCs and production of growth factors and stromal components related to tumor-stromal interactions.
|
Report
(3 results)
Research Products
(3 results)
