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首页> 外文期刊>Molecular and Cellular Biology >Transfection of the EJ rasHa gene into keratinocytes derived from carcinogen-induced mouse papillomas causes malignant progression.
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Transfection of the EJ rasHa gene into keratinocytes derived from carcinogen-induced mouse papillomas causes malignant progression.

机译：将EJ Rasha基因转染到来自致癌癌乳头瘤的角质形成细胞导致恶性进展。

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摘要

The development of malignant tumors in carcinogen-treated mouse skin appears to involve several genetic changes. Genetic changes which initiate the process are believed to induce alterations in the normal pattern of epidermal differentiation, resulting in the formation of benign tumors, i.e., epidermal papillomas. Subsequent changes appear to be required for the malignant conversion of papillomas to epidermal, squamous-cell carcinomas. Activation of the rasHa gene occurs frequently in chemically induced benign skin papillomas as well as squamous cell carcinomas and thus may represent one mechanism to achieve the initiation step. In the present study, we analyzed several cell lines derived from chemically induced mouse skin papillomas for the presence of transforming oncogenes by transfection of their DNA into NIH 3T3 cells. These papilloma cell lines exhibit an altered differentiation program, i.e., the ability to proliferate under culture conditions favoring terminal differentiation. When DNA from six separate cell lines was tested in the NIH 3T3 transfection assay, active transforming activity was not detected. However, when the EJ rasHa gene was introduced into three of the papilloma cell lines by DNA transfection, transfectants showed an enhanced capacity to proliferate under differentiating culture conditions and formed rapidly growing, anaplastic carcinomas in nude mice. Our findings suggest that in some papilloma cells, a genetic change distinct from rasHa activation may produce an altered differentiation program associated with the initiation step, and this genetic alteration may act in a cooperating fashion with an activated ras gene to result in malignant progression.
机译：致癌物理小鼠皮肤中恶性肿瘤的发展似乎涉及几种遗传变化。发起该方法的遗传变化被认为诱导表皮分化的正常模式的改变，从而形成良性肿瘤的形成，即表皮乳头瘤。乳头瘤的恶性转化对表皮的恶性转化，乳头鳞状细胞癌的后续变化似乎是必需的。 Rasha基因的激活经常发生在化学诱导的良性皮肤乳头瘤中以及鳞状细胞癌中，因此可以代表一种实现引发步骤的一种机制。在本研究中，我们分析了几种来自化学诱导的小鼠皮骨乳头瘤的细胞系，用于通过将其DNA转染到NIH 3T3细胞中转化癌细胞。这些乳头瘤细胞系具有改变的分化计划，即在有利的肠子分化下促进培养条件的能力。当在NIH 3T3转染测定中测试来自六个单独的细胞系的DNA时，未检测到活性转化活性。然而，当通过DNA转染将EJ Rasha基因引入三种乳头瘤细胞系中时，转染剂在区分培养条件下促进了增强的能力，并在裸鼠中形成了快速生长的促进癌癌。我们的研究结果表明，在一些乳头瘤细胞中，不同于Rasha激活的遗传变化可以产生与引发步骤相关的改变的分化计划，并且该遗传改变可以用活化的RAS基因以合作的方式作用，以导致恶性进展。

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