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首页> 外文期刊>Molecular and Cellular Biology >Tumorigenicity of the met proto-oncogene and the gene for hepatocyte growth factor.
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Tumorigenicity of the met proto-oncogene and the gene for hepatocyte growth factor.

机译：癌基因原癌基因和肝细胞生长因子基因的致瘤性。

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摘要

The met proto-oncogene is the tyrosine kinase growth factor receptor for hepatocyte growth factor/scatter factor (HGF/SF). It was previously shown that, like the oncogenic tpr-met, the mouse met proto-oncogene transforms NIH 3T3 cells. We have established NIH 3T3 cells stably expressing both human (Methu) and mouse (Metmu) met proto-oncogene products. The protein products are properly processed and appear on the cell surface. NIH 3T3 cells express endogenous mouse HGF/SF mRNA, suggesting an autocrine activation mechanism for transformation by Metmu. However, the tumor-forming activity of Methu in NIH 3T3 cells is very low compared with that of Metmu, but efficient tumorigenesis occurs when Methu and HGF/SFhu are coexpressed. These results are consistent with an autocrine transformation mechanism and suggest further that the endogenous murine factor inefficiently activates the tumorigenic potential of Methu. The tumorigenicity observed with reciprocal chimeric human and mouse receptors that exchange external ligand-binding domains supports this conclusion. We also show that HGF/SFhu expressed in NIH 3T3 cells produces tumors in nude mice.
机译：原始的癌基因是肝细胞生长因子/分散因子（HGF / SF）的酪氨酸激酶生长因子受体。先前已证明，与致癌的tpr-met一样，小鼠遇到的原癌基因转化了NIH 3T3细胞。我们已经建立了稳定表达人（Methu）和小鼠（Metmu）遇到的原癌基因产物的NIH 3T3细胞。蛋白质产品经过适当处理，并出现在细胞表面。 NIH 3T3细胞表达内源性小鼠HGF / SF mRNA，暗示了Metmu进行转化的自分泌激活机制。然而，与Metmu相比，Methu在NIH 3T3细胞中的肿瘤形成活性非常低，但是当Methu和HGF / SFhu共表达时，会发生有效的肿瘤发生。这些结果与自分泌转化机制一致，并且进一步表明内源鼠因子不能有效地激活甲硫氨酸的致瘤潜力。用交换外部配体结合结构域的相互嵌合人类和小鼠受体观察到的致瘤性支持这一结论。我们还显示在NIH 3T3细胞中表达的HGF / SFhu在裸鼠中产生肿瘤。

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