HPV-16 E6 和 E7 癌基因的表达因 Mdm2 敲低而下调。
HPV-16 E6 and E7 oncogene expression is downregulated as a result of Mdm2 knockdown.
机构信息
Department of Clinic Analysis and Molecular Diagnostic, Faculty of Chemistry, Universidad Autónoma de Coahuila, Republica Oriente, CP 25280, Saltillo, Coahuila, Mexico.
出版信息
Int J Oncol. 2012 Jul;41(1):141-6. doi: 10.3892/ijo.2012.1429. Epub 2012 Apr 10.
The carcinogenic potential of HPV infections is based on the integration and constitutive expression of the E6 and E7 genes which inhibit the p53 and Rb tumor suppressor proteins. In normal cells, Mdm2 regulates p53 in a negative feedback loop, and although Mdm2 is apparently functional in HPV-infected cells, E6 is the protein responsible for repressing p53 replacing Mdm2 function. The role of Mdm2 in HPV-positive cells is still elusive. In this study, Mdm2 was knocked down in an HPV-positive cervical cancer cell line; as a result we found downregulation of the expression of E6 and E7 and p53 upregulation.
HPV 感染的致癌潜能基于 E6 和 E7 基因的整合和组成型表达，这些基因抑制 p53 和 Rb 肿瘤抑制蛋白。在正常细胞中，Mdm2 在负反馈环中调节 p53，尽管 Mdm2 在 HPV 感染细胞中显然是有功能的，但 E6 是负责抑制 p53 从而取代 Mdm2 功能的蛋白。Mdm2 在 HPV 阳性细胞中的作用仍不清楚。在这项研究中，我们在 HPV 阳性宫颈癌细胞系中敲低了 Mdm2，结果发现 E6 和 E7 的表达下调和 p53 的上调。
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