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目的 探讨野生型 p5 3 (wtp5 3 )、Fas/FasL在提高肝癌细胞化疗药物敏感性中的作用及其机制。方法 用化疗药物争光霉素 60 0mg/L分别处理人肝癌细胞株HepG2、Hep3B和PLC/PRF/5 ,观察争光霉素对肝癌细胞Fas/FasL表达的影响 ;预先将携带wtp5 3基因的重组腺病毒分别感染人肝癌细胞株 2 4h ,再用争光霉素进行诱导 ,观察感染前后肝癌细胞Fas/FasL的表达变化 ,并对经上述处理前后的肝癌细胞进行凋亡检测。结果 单纯争光霉素 60 0mg/L诱导虽可提高肝癌细胞FasL的表达 ,但对其Fas的表达并无明显作用 ;感染wtp5 3基因后再应用争光霉素(60 0mg/L) ,则肝癌细胞Fas/FasL的表达水平不仅显著高于单纯争光霉素组 ,同时自身也发生了明显凋亡。结论 wtp5 3基因可能是通过上调肝癌细胞Fas/FasL的表达来降低其自身的凋亡阈值 ,进而提高肝癌细胞对化疗药物的敏感性 ,Fas/FasL在wtp5 3基因逆转肝癌细胞耐药性中具有一定的作用。
Objective To investigate the role and mechanism of wild-type p53 (wtp5 3 ) and Fas/FasL in improving the sensitivity of chemotherapeutic drugs in hepatocellular carcinoma cells. Methods Human hepatocellular carcinoma cell lines HepG2, Hep3B and PLC/PRF/5 were treated with the chemotherapeutic drug bleomycin 600 mg/L. The effect of bleomycin on the expression of Fas/FasL in hepatocellular carcinoma cells was observed. The recombinant adenocarcinoma carrying the wtp5 3 gene was used in advance. The virus was infected with human hepatocellular carcinoma cell line for 24 hours, and then induced with bleomycin. The expression of Fas/FasL in hepatoma cells before and after infection was observed, and the apoptosis of hepatoma cells before and after treatment was detected. Results The expression of FasL in hepatocellular carcinoma cells was enhanced by the induction of bleomycin 600 mg/L, but there was no significant effect on the expression of Fas. After the infection of wtp5 3 gene with the administration of bleomycin (60 mg/L), the hepatoma cells The expression level of Fas/FasL was not only significantly higher than that of bleomycin alone, but also had obvious apoptosis. Conclusion The wtp5 3 gene may reduce its own apoptosis threshold by up-regulating the expression of Fas/FasL in hepatoma cells, and then increase the sensitivity of hepatoma cells to chemotherapeutic drugs. Fas/FasL has a role in reversing the drug resistance of hepatoma cells by wtp5 3 gene. A certain role.