Abstract: Objective To acquire anti tumor target drug basic research data,we investigated the difference in Src/MAPK signal transduction pathway of human pancreatic cancer cell line HPACand BxPC-3.Methods HPACand BxPC-3 were cultured in RPMI 1640 and the same cell number divided into four groups:control,TGF-α,TGF-α+PP2 and TGF-α+PD.Cells were changed to serum free medium in condition of cell adhesion and 70% confluency and cultured 48 h.Control were treated by serum free medium;TGF-α group were treated 2 h by final concretion 7nmol/L TGF-α in serum free medium;TGF-α+PP2 group were treated 20 min by final concretion 10 μmol/L PP2 and then 2 h by final concretion 7nmol/L TGF-α;TGF-α+ PDgroup were treated 20 min by final concretion 30 μmol/L PD and then 2 h by final concretion 7 nmol/L TGF-α.The expression of pp60c-Src and pERK1/2 were analyzed by Western bloting.Results The expression of pp60c-Src in cell line HPACin control significantly higher than TGF-α group,TGF-α+PDgroup(P<0.05)and TGF-α+PP2 group(P<0.01);The expression of pERK1/2 in HPACin TGF-α group were significantly higher than that of control and TGF-α+PDgroup(P<0.01),but no significantly difference to that of TGF-α+PP2group(P>0.05).pp60c-Src expression of TGF-α group in BxPC-3 were significantly higher than that of control(P<0.05),and that of TGF-α+ PP2 group(P<0.01),but not significantly different to that of TGF-α+PDgroup(P>0.05);The expression of pERK1/2 of TGF-α group in BxPC-3 were significantly higher than that of control,TGF-α+PDgroup and TGF-α+PP2 group(P<0.01).Conclusion There were some difference in Src/MAPK signal transduction pathway between human pancreatic cancer cell line HPAC and BxPC-3.We supposed c-src is key signal molecular in activation of Ras/Raf/MAPK pathway in human pancreatic cancer cell line BxPC-3.The mechanism of c-src in human pancreatic cancer cell line HPAC should advanced explored.

Key words: human pancreatic cancer cell line, HPAC, BxPC-3, Src, MAPK