The development of pancreatic cancer therapy based on regulating pancreatic cancer desmoplasia by targeting pancreatic stellate cells to improve drug delivery

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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.