RESUMO
Objective To investigate the inhibitory effect of cucurmosin (CUS) combined with the commonly used chemotherapeutic drugs for pancreatic cancer in clinical practice including Gemcitabine (GEM),Fluorouracil (5-FU),Paclitaxel (PTX) and Cisplatin (DDP) on cell proliferation of human pancreatic cancer cell line BxPC-3.Mehtods Sulforhodamine B (SRB) assay was used to detect the inhibition on the cell proliferation of BxPC-3 cells in vitro after the treatment of CUS combined with GEM,5-FU,PTX and DDP,respectively.Colony formation assay was also conducted and Jin' s formula was used to assess the synergistic effect of these combinations.Results The inhibition rate of CUS combined with GEM,5-FU,PTX and DDP were all higher than those of each drug alone (q ＞ 0.85),which became obvious in low concentrations.The colony formation inhibition rate of CUS combined with GEM,5-FU,PTX or DDP were all higher than each single drug treatment (q ＞ 1.15).Conclusion CUS could enhance the cell growth inhibition of GEM,5-FU,PTX and DDP in BxPC-3 cells in vitro with a good synergistic effect.
RESUMO
Objective To investigate the mechanisms involved in cucurmosin-induced apoptosis of pancreatic cancer cell SW1990.Methods The expression of EGFR,PI3K,Akt,Bad,Caspase -9,mTOR,P70S6K-α,and 4E BP1 at the protein level were detected by western blot analysis,and RTPCR was used to determine EGFR mRNA expression.Results An increased concentration of cucurmosin showed a subsequent decrease in the expression of EGFR,PI3K,Akt,mTOR,P70S6Kα,and 4E -BP1,whereasthe expression of Bad and Caspase-9 were elevated.However,the mRNA expression of EGFR was unchanged.Conclusion Cucurmosin is shown to induce the apoptosis of pancreatic cancer cell SW1990 by down regulating the expression of EGFR and thus inactivating the PI3K/Akt/mTOR signaling pathway.