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首页> 外文期刊>Molecular and Cellular Biology >The Absence of p53 Promotes Metastasis in a Novel Somatic Mouse Model for Hepatocellular Carcinoma
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The Absence of p53 Promotes Metastasis in a Novel Somatic Mouse Model for Hepatocellular Carcinoma

机译：p53的缺乏促进肝细胞癌的新型体细胞小鼠模型中的转移。

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We have generated a mouse model for hepatocellular carcinoma using somatic delivery of oncogene-bearing avian retroviral vectors to the liver cells of mice expressing the viral receptor TVA under the control of the albumin gene promoter (Alb-TVA mice). Viruses encoding mouse polyoma virus middle T antigen (PyMT) induced tumors, which can be visualized with magnetic resonance imaging, in 65% of TVA-positive animals. While these tumors can exceed 10 mm in diameter, they do not invade locally or metastasize to the lungs. Delivery of PyMT-expressing viruses to Alb-TVA mice lacking an intact p53 gene does not increase tumor incidence. However, the resulting tumors are poorly differentiated, invasive, and metastatic to the lungs. Gene expression microarrays identified over 100 genes that are differentially expressed between tumors found in p53 wild-type and p53 null mice. Some of these genes, such as cathepsin E and Igf2, have been previously implicated in tumor cell migration and invasion. Tumors induced in p53 null, TVA transgenic mice by PyMT mutants with changes in specific tyrosine residues fail to form metastases, indicating that metastasis is dependent on both the oncogene and the absence of p53.
机译：我们已经使用携带癌基因的禽逆转录病毒载体向表达白蛋白基因启动子控制的表达病毒受体TVA的小鼠（Alb-TVA小鼠）的肝细胞中体细胞递送了肝癌的小鼠模型。编码小鼠多瘤病毒中T抗原（PyMT）诱导的肿瘤的病毒，可以在65％的TVA阳性动物中通过磁共振成像观察到。尽管这些肿瘤的直径可能超过10毫米，但它们不会局部侵入或转移到肺部。将表达PyMT的病毒传递给缺乏完整 p53 基因的Alb-TVA小鼠不会增加肿瘤发生率。但是，由此产生的肿瘤分化差，侵袭性强，并转移到肺部。基因表达微阵列鉴定了在 p53 野生型和 p53 无基因小鼠中发现的肿瘤之间差异表达的100多个基因。这些基因中的某些，例如 cathepsin E 和 Igf2 ，以前已被认为与肿瘤细胞的迁移和侵袭有关。在PemMT突变体中，酪氨酸残基发生变化的PyMT突变体在 p53 空TVA转基因小鼠中诱导的肿瘤未能形成转移灶，表明转移取决于癌基因和 p53 。

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