2002Zhonghua shiyan waike zazhiRequires access

The role of wtp53 and Fas/FasL in the process of sensitizing hepatoma cells to chemotherapy

Liu Yan-jun

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Abstract

Objective To investigate the role of p53 and Fas/FasL in the process of sensitizing hepatoma cells to chemotherapy.Methods Human hepatoma cell lines HepG2,Hep3B and PLC/PRF/5 were treated respectively with a chemotherapeutic drug (bleomycin) at various concentrations (0 600?mg/L).The expression of Fas/FasL in hepatoma cell lines was detected after treatment with bleomycin or in combination with infection with a recombinant adenoviral vector expressing wide type (wt) p53 gene (Ad p53).Then,effect of Fas/FasL on the apoptosis in hepatoma cell lines themselves was examined.Results Bleomycin(0 600?mg/L)did not suppress the growth of hepatoma cell lines,and the same dosage had a stimulatory effect on FasL and no apparent regulation of Fas.However,treatment with bleomycin following infection with Ad p53 could significantly increase the expression of Fas/FasL in the hepatoma cell lines and therefore render these cells more sensitive to chemotherapeutic drug via Fas mediated apoptosis,compared to single chemotherapy.Conclusion Apoptosis induced by bleomycin is mediated in part by wt p53 dependent stimulation of Fas/FasL system and reverse the hepatoma cell's drug resistance.The Fas/FasL may play a role in the reversal effects of the drug resistant hepatoma cell lines by wtp53.

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Objective To investigate the role of p53 and Fas/FasL in the process of sensitizing hepatoma cells to chemotherapy.Methods Human hepatoma cell lines HepG2,Hep3B and PLC/PRF/5 were treated respectively with a chemotherapeutic drug (bleomycin) at various concentrations (0 600?mg/L).The expression of Fas/FasL in hepatoma cell lines was detected after treatment with bleomycin or in combination with infection with a recombinant adenoviral vector expressing wide type (wt) p53 gene (Ad p53).Then,effect of Fas/FasL on the apoptosis in hepatoma cell lines themselves was examined.Results Bleomycin(0 600?mg/L)did not suppress the growth of hepatoma cell lines,and the same dosage had a stimulatory effect on FasL and no apparent regulation of Fas.However,treatment with bleomycin following infection with Ad p53 could significantly increase the expression of Fas/FasL in the hepatoma cell lines and therefore render these cells more sensitive to chemotherapeutic drug via Fas mediated apoptosis,compared to single chemotherapy.Conclusion Apoptosis induced by bleomycin is mediated in part by wt p53 dependent stimulation of Fas/FasL system and reverse the hepatoma cell's drug resistance.The Fas/FasL may play a role in the reversal effects of the drug resistant hepatoma cell lines by wtp53.

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Available abstract

Objective To investigate the role of p53 and Fas/FasL in the process of sensitizing hepatoma cells to chemotherapy.Methods Human hepatoma cell lines HepG2,Hep3B and PLC/PRF/5 were treated respectively with a chemotherapeutic drug (bleomycin) at various concentrations (0 600?mg/L).The expression of Fas/FasL in hepatoma cell lines was detected after treatment with bleomycin or in combination with infection with a recombinant adenoviral vector expressing wide type (wt) p53 gene (Ad p53).Then,effect of Fas/FasL on the apoptosis in hepatoma cell lines themselves was examined.Results Bleomycin(0 600?mg/L)did not suppress the growth of hepatoma cell lines,and the same dosage had a stimulatory effect on FasL and no apparent regulation of Fas.However,treatment with bleomycin following infection with Ad p53 could significantly increase the expression of Fas/FasL in the hepatoma cell lines and therefore render these cells more sensitive to chemotherapeutic drug via Fas mediated apoptosis,compared to single chemotherapy.Conclusion Apoptosis induced by bleomycin is mediated in part by wt p53 dependent stimulation of Fas/FasL system and reverse the hepatoma cell's drug resistance.The Fas/FasL may play a role in the reversal effects of the drug resistant hepatoma cell lines by wtp53.

Key concepts: Fas ligand, Bleomycin, Apoptosis, Cell culture, Cancer research, Cell, Chemotherapy, Biology

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