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[目的]探讨重组腺病毒p53(rAd-p53)影响口腔黏膜异常增生细胞(POE-9n)生长、诱导凋亡的分子机制。[方法]利用RT-PCR及Westernblot技术检测rAd-p53转染POE-9n细胞后p53、p21CIP/WAF及bcl-2mRNA和蛋白的表达变化。[结果]POE-9n细胞经rAd-p53转染后,p53、p21CIP/WAF和bcl-2mRNA和蛋白水平的表达均出现明显变化。转染24h后,p53、p21CIP/WAFmRNA及蛋白表达显著增高(P<0.01),而bcl-2则在转染72h后表达明显降低(P<0.01)。[结论]rAd-p53转染POE-9n细胞后,外源性p53的导入使p21CIP/WAF激活,并抑制bcl-2的表达,从而诱导细胞凋亡。
[Objective] To investigate the molecular mechanism of recombinant adenovirus p53 (rAd-p53) affecting the growth and inducing apoptosis of oral dysplastic cells (POE-9n). [Methods] The expression of p53, p21CIP / WAF and bcl-2 mRNA and protein in POE-9n cells transfected with rAd-p53 were detected by RT-PCR and Western blot. [Results] The expression of p53, p21CIP / WAF and bcl-2 mRNA and protein in POE-9n cells after transfection with rAd-p53 all showed obvious changes. The expression of p53, p21CIP / WAF mRNA and protein were significantly increased (P <0.01) 24h after transfection, while the expression of bcl-2 was significantly decreased 72h after transfection (P <0.01). [Conclusion] After transfection of POE-9n cells with rAd-p53, exogenous p53 can activate p21CIP / WAF and inhibit the expression of bcl-2, thereby inducing cell apoptosis.