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为探讨抗癌基因在肿瘤治疗中作用的可能性，以反转录病毒N2A为载体，将p53cDNA及顺式作用元件反向插入N2A两端LTR间的XhoⅠ位点，获得了野生型p53基因反转录病毒重组体。将该病毒重组体转染单向性包装细胞系ψ－2和双向性包装细胞系PA317）筛选后扩增有抗性的细胞克隆，用其产生的新鲜病毒颗粒感染p53基因表达异常的人喉癌细胞系（Hep2）。发现有前病毒整合的受体细胞，细胞染色质浓缩周边化，细胞肿胀，出现凋亡小体，基因组DNA电泳图谱呈阶梯状改变。结果表明反转录病毒介导的野生型p53基因能不同程度地诱导人喉癌细胞凋亡。
To explore the possibility of the role of anticancer genes in tumor therapy, the retroviral N2A was used as a vector to reversely insert the p53 cDNA and cis-acting elements into the XhoI site between the LTRs on both ends of N2A, and the wild-type p53 gene was obtained. Transcriptional virus recombinants. The viral recombinant was transfected with the unidirectional packaging cell line ψ-2 and the bidirectional packaging cell line PA317. After screening, a resistant cell clone was amplified, and the p53 gene expression abnormal human larynx was infected with the fresh virus particles produced by the virus. Cancer cell line (Hep2). Recipient cells with previral integration were found. Cell chromatin was concentrated and peripheralized. The cells were swollen and apoptotic bodies appeared. The electrophoretogram of genomic DNA was changed stepwise. The results showed that retrovirus-mediated wild-type p53 gene can induce apoptosis of human laryngeal carcinoma cells to varying degrees.