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PENG Lin-tao, XU Xin. Effect of Fas,bcl-2 and caspase8 on Norcantharidin Induced Esophageal Cancer Cell Line Eca-109 Apotosis and Molecular Mechanism[J]. Cancer Research on Prevention and Treatment, 2010, 37(04): 398-401. DOI: 10.3971/j.issn.1000-8578.2010.04.008
Citation: PENG Lin-tao, XU Xin. Effect of Fas,bcl-2 and caspase8 on Norcantharidin Induced Esophageal Cancer Cell Line Eca-109 Apotosis and Molecular Mechanism[J]. Cancer Research on Prevention and Treatment, 2010, 37(04): 398-401. DOI: 10.3971/j.issn.1000-8578.2010.04.008

Effect of Fas,bcl-2 and caspase8 on Norcantharidin Induced Esophageal Cancer Cell Line Eca-109 Apotosis and Molecular Mechanism

  • Objective To investigate the effect of Fas、bcl-2、caspase 8 on Norcantharidin inhibiting proliferation of Eca-109 cells and inducing its apoptosis and the possible molecule mechanism. Methods The morphology was detected by inverted microscope. The apoptosis and proliferation index of cells were analysed by FCM.The expression of apoptosis associated proteins Fas、bcl-2、caspase8 was measured by immunocytochemical staining. Results The inverted microscope showed that Norcantharidin caused morphological changes of Eca-109 cells. The apoptosis cells were observed on a DNA histogram as subdiploid or pre-G1 peak. The cell cycle distribution changed obviously with treatment of norcantharidin.Immunocytochemical staining showed that the expressions of Fas and caspase 8 protein were induced significantly while the expression of bcl-2 protein was reduced on Eca-109 cells after treated by norcantharidin(P<0.05). Conclusion Norcantharidin may inhibit Eca-109 cell proliferation and induce its apoptosis.The possible mechanism may be related with up-regulating the expressions of Fas、caspase8 and down-regulating the expression of bcl-2 protein.
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