Transgenic mouse model for skin malignant melanoma
Transgenic mouse model for skin malignant melanoma
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DOI：
10.1038/sj.onc.1202077
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发表时间：
1998-10-08
期刊：
影响因子：
8
通讯作者：
Nakashima, I
中科院分区：
文献类型：
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作者：
Kato, M;Takahashi, M;Nakashima, I
我们在这里报告一种新的金属硫蛋白-I（MT）/ret转基因小鼠系，皮肤黑变病，良性黑色素细胞肿瘤和恶性黑色素瘤转移到远处器官逐步发展。肿瘤的发展和恶性转化的过程中，在这行可能类似于人类巨大的先天性黑色素细胞痣，是目前在出生时，并经常引起恶性黑色素瘤在衰老过程中。我们观察到在疾病进展过程中ret转基因的表达水平和活性增加。转基因表达的增加伴随着丝裂原活化蛋白激酶（MAPK）和c-Jun以及基质金属蛋白酶的激活。这些结果表明，进行性失调的ret转基因的表达水平可能发挥了至关重要的作用，在MT/ret转基因小鼠系的黑素细胞肿瘤的恶性转化。
We report here on a novel metallothionein-I (MT)/ret transgenic mouse line in which skin melanosis, benign melanocytic tumor and malignant melanoma metastasizing to distant organs develop stepwise. The process of tumor development and its malignant transformation in this line may resemble that of the human giant congenital melanocytic nevus that is present at birth and that frequently gives rise to malignant melanoma during aging. We observed an increase in the expression level and activity of the ret transgene during the disease progression. That increase in transgene expression accompanied an activation of mitogen-activated protein kinases (MAPKs) and c-Jun as well as matrix metalloproteinases. These results suggest that progressive dysregulation of the expression level of the ret transgene might play a crucial role in the malignant transformation of melanocytic tumors developed in the MT/ret transgenic mouse line.