卡铂诱导卵巢癌细胞株OVCA_3凋亡中p63及p53基因mRNA的变化

Expression of p63 and p53 at mRNA level after apoptosis induced by caboplatin

目的探讨卡铂诱导人卵巢癌细胞株OVCA_3凋亡后p63、p53基因mRNA的变化及二者的相关性。方法四唑盐比色法测细胞的存活率,实时荧光定量反转录聚合酶链反应法检测卡铂诱导OVCA_3凋亡后p63、p53基因mRNA的变化。结果卡铂能明显抑制OVCA_3的生长,其作用时间与细胞生长抑制率呈明显正相关,低浓度卡铂(10μg/mL)对OVCA_3生长抑制率明显低于高浓度卡铂(25μg/mL,P<0.05),随着OVCA_3凋亡率增加,存活的细胞中p63和p53基因mRNA的表达水平也逐渐增加,且高浓度卡铂处理后,存活的卵巢癌细胞中p63和p53基因mRNA的表达量均明显高于阴性对照和低浓度作用组(P<0.05),差异有统计学意义。结论 p63、p53基因共同参与卵巢癌耐药环节,二者在卡铂作用后发挥的作用是一致的。

Objective To study the variable at mRNA level in apoptosis induced by caboplatin, the possibility of p63 involved chemoresistance of caboplatin and the primary relationship between p53 and p63.Methods The apoptosis was induced by caboplatin and the mRNA of p63,p53 were investigated by real-time fluorescence quantitative reverse transcription-polymerase chain reaction.Results Caboplatin could inhibit OVCA_3 cells growth in dose-and time-dependent manner.The low concentration had less effect than the high concentration.p53 and p63 mRNA in the survival cells increased gradually following OVCA_3 apoptosis increase.Conclusion p53, p63 biology-effects carry out through cell apoptosis.p63 and mu-p53 carry out oncogence function. p63,p53 involve in chemoresistance.The functions of p63,p53 involve in multilayer.