AIM:To explore the mechanisms of effects of oil A onapoptosis of human pancreatic cancer cells.METHODS:Cellular DNA content was analyzed by flowcytometry.Western blotting was used for caspase-3 andPARP,caspase-7,caspase-9,cytochrome c,Bcl-2,Bax,Mcl-1,cyclinA,cyclin B1,cyclin D1,cyclin E,CDK2,CDK4,CDK6,P21,P27,GADD45,GADD153.RESULTS:The caspase-3,caspase-7,and caspase-9activities were significantly increased as well as the cleavageof caspase-3,downstream substrate poly-ADP ribosepolymerase(PARP)was induced.The amount of cytochromec in the cytosolic fraction was increased,while the amountof cytochrome c in the mitochondrial fraction was decreasedafter oil A treatment.The anti-apoptosis proteins Bcl-2and Mcl-1 were decreased in parallel and Bax increased,indicating that Bcl-2 family proteins-mitochondria-caspasecascade was responsible for oil-induced apoptosis.Theproportion of cells in the G0/G1 decreased in MiaPaCa-2and AsPC-1 cells after the treatment of oil A for 24 hours.The number of cells in S phase was increased in two cancercell lines at 24 hours.Therefore,cells were significantlyaccumulated in G2/M phase.The cells with a sub-G0/G1DNA content,a hallmark of apoptosis,were seen at 24 hoursboth in MiaPaCa-2 and AsPC-1 cells following exposure tooil A.The expression of cyclin A and cyclin B1 was slightlydecreased and cyclin D1 levels were markedly lowered inMiaPaCa-2 cells.The expression of cyclin A and cyclin B1was markedly decreased and cyclin D1 levels were slightlylowered in AsPC-1 cells,while cyclin E was not affected andthe levels of CDK2,CDK4,and CDK6 were unchanged inMiaPaCa-2 and AsPC-1 cells.In response to oil A,P21expression was increased,but P27 expression was notaffected.The expression of both GADD45 and GADD153was increased in two cell lines following oil A treatment. CONCLUSION: Oil A induces apoptosis of pancreatic cancer cells via activating caspase cascade, modifying cell cycle progress and changing cell cycle-regulating proteins and GADD expression. AIM: To explore the mechanisms of effects of oil A onapoptosis of human pancreatic cancer cells. METHODS: Cellular DNA content was analyzed by flow cytometry. Western blotting was used for caspase-3 and PARP, caspase-7, caspase-9, cytochrome c, Bcl -2, Bax, Mcl-1, cyclinA, cyclin B1, cyclin D1, cyclin E, CDK2, CDK4, CDK6, P21, P27, GADD45, GADD153.RESULTS: The caspase-3, caspase-7, and caspase-9activities were The increased amount of cytochrome c in the cytosolic fraction was increased, while the amount of cytochrome c in the mitochondrial fraction was decreased after oil A treatment. anti-apoptosis proteins Bcl-2 and Mcl-1 were decreased in parallel and Bax increased, indicating that Bcl-2 family proteins-mitochondria-caspase cascade was responsible for oil-induced apoptosis. The proportion of cells in the G0 / G1 decreased in MiaPaCa- 2 and AsPC-1 cells after the treatment of oil A for 24 hours. Number of cells in S phase was increased in two cancer cells line at 24 hours.Therefore, cells were significantlyaccumulated in G2 / Mphase.The cells with a sub-G0 / G1DNA content, a hallmark of apoptosis, were seen at 24 hoursboth in MiaPaCa-2 and AsPC-1 cells following exposure tooil A. The expression of cyclin A and cyclin B1 was slightly decreased and cyclin D1 levels were markedly lowered in MiPaCa-2 cells. The expression of cyclin A and cyclin B1 was markedly decreased and cyclin D1 levels were slightlylowered in AsPC -1 cells, while cyclin E was not affected and the levels of CDK2, CDK4, and CDK6 were unchanged in MiaPaCa-2 and AsPC-1 cells. In response to the oil A, P21 expression was increased, but P27 expression was not affected. The expression of both GADD45 and GADD153 was increased in two cell lines following oil A treatment. CONCLUSION: Oil A induces apoptosis of pancreatic cancer cells via activating caspase cascade, modifying cell cycle progress and changing cell cycle-regulating proteins and GADD expression.