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首页> 外文OA文献 >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：EJ rasHa基因转染到源自致癌物诱导的小鼠乳头状瘤的角质形成细胞中会导致恶性进展。

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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：致癌物处理过的小鼠皮肤中恶性肿瘤的发展似乎涉及一些遗传变化。据信引发该过程的遗传改变引起表皮分化正常模式的改变，导致良性肿瘤，即表皮乳头状瘤的形成。乳头状瘤恶变为表皮鳞状细胞癌似乎需要随后的改变。 rasHa基因的激活经常发生在化学诱导的良性皮肤乳头状瘤以及鳞状细胞癌中，因此可能代表实现起始步骤的一种机制。在本研究中，我们分析了从化学诱导的小鼠皮肤乳头状瘤衍生的几种细胞系中是否存在通过将其DNA转染到NIH 3T3细胞中而转化的癌基因。这些乳头瘤细胞系表现出改变的分化程序，即在有利于终末分化的培养条件下增殖的能力。在NIH 3T3转染试验中测试了来自六个不同细胞系的DNA时，未检测到活性转化活性。但是，当通过DNA转染将EJ rasHa基因引入到三个乳头瘤细胞系中时，转染子在分化的培养条件下显示出增强的增殖能力，并在裸鼠中形成快速生长的间变性癌。我们的发现表明，在一些乳头瘤细胞中，不同于rasHa激活的遗传变化可能会产生与起始步骤相关的分化程序，并且这种遗传变化可能与激活的ras基因协同作用，导致恶性进展。

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