TPR-MET癌基因的转基因表达会导致乳腺增生和肿瘤的发生。
Transgenic expression of tpr-met oncogene leads to development of mammary hyperplasia and tumors.
作者信息
Liang T J, Reid A E, Xavier R, Cardiff R D, Wang T C
机构信息
Department of Medicine, Massachusetts General Hospital, Boston 02114, USA.
出版信息
J Clin Invest. 1996 Jun 15;97(12):2872-7. doi: 10.1172/JCI118744.
Abstract
Receptor tyrosine kinases are important in cell signal transduction and proliferation. Abnormal expression of tyrosine kinases often leads to malignant transformation. C-met is a tyrosine kinase receptor and its ligand is hepatocyte growth factor (HGF). HGF/c-met plays diverse role in regulation of cell growth, shape and movement. Constitutively activated met, such as tpr-met, is a potent oncogene in vitro, but its carcinogenic role in vivo remains unclear. Our study demonstrates that expression of tpr-met leads to development of mammary tumors and other malignancies in transgenic mice, and suggests that deregulated met expression may be involved in mammary carcinogenesis.
摘要
受体酪氨酸激酶在细胞信号转导和增殖中起重要作用。酪氨酸激酶的异常表达常导致恶性转化。C-甲硫氨酸是一种酪氨酸激酶受体，其配体是肝细胞生长因子（HGF）。HGF/C-甲硫氨酸在调节细胞生长、形态和运动中发挥多种作用。持续激活的甲硫氨酸，如tpr-甲硫氨酸，在体外是一种有效的致癌基因，但其在体内的致癌作用仍不清楚。我们的研究表明，tpr-甲硫氨酸的表达导致转基因小鼠乳腺肿瘤和其他恶性肿瘤的发生，并提示甲硫氨酸表达失调可能与乳腺癌发生有关。
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