| Project/Area Number |
23659652
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Digestive surgery
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| Research Institution | Kyushu University |
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Principal Investigator |
NAGAI Eishi 九州大学, 医学研究院, 准教授 (30264021)
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| Co-Investigator(Kenkyū-buntansha) |
INOUE Shigetaka 九州大学, 医学研究院, 共同研究員 (00529802)
ONIMARU Manabu 九州大学, 医学研究院, 共同研究員 (80529876)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 膵癌 / 膵星細胞 / ピルフェニドン / desmoplasia / pancreatic cancer / pirfenidone / gemcitabine / periostin |
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| Research Abstract |
We indentified that the antifibrotic agent pirfenidone could suppress desmoplasia and exert anti-tumor effects against pancreatic cancer. In vitro, pirfenidone inhibited the proliferation, invasiveness, and migration of pancreatic stellate cells and tumor-stromal interaction between pancreatic stellate cells and pancreatic cancer cells. Oral administration of pirfenidone to the mice, which implanted with pancreatic cancer cells and pancreatic stellate cells, significantly reduced tumor growth. Pirfenidone also decreased the proliferation of pancreatic stellate cells, and inhibited the deposition of collagen type I and periostin in tumors. Pirfenidone in combination with gemcitabine more effectively suppressed tumor growth compared with pirfenidone or gemcitabine alone. Our findings indicate that pirfenidone is a promising antitumor agent for pancreatic cancer, owing to its suppression of desmoplasia through regulating pancreatic cancer cells.
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