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首页> 外文期刊>European Journal of Cell Biology: Journal of Deutsche Gesellschaft fur Elektronenmikroskopie: Journal of Deutsche Gesellschaft fur Zellbiologie >Chemical reverse transformation of CHO-K1 cells induces changes inexpression of a candidate tumour suppressor and of a gene not previouslycharacterised as transformation related
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Chemical reverse transformation of CHO-K1 cells induces changes inexpression of a candidate tumour suppressor and of a gene not previouslycharacterised as transformation related

机译：CHO-K1细胞的化学反向转化诱导候选肿瘤抑制基因和先前未表征为转化相关基因的表达变化

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摘要

Chemical reverse transformation of CHO-K1 and other cells is a well-established phenomenon, in which oncogenically transformed cells re-acquire fibroblastoid morphology, contact inhibition and anchorage-dependent growth, in response to cyclic AMP and other agents. A limited number of changes in gene transcription and enzyme activity have been demonstrated to coincide with these morphological and physiological changes. We have used a partial differential display to identify four genes that are transcriptionally modulated in reverse transformation. One of these, encoding ribosomal protein S18, is transcriptionally suppressed, probably as a result of the detransforming process. Three others are transcriptionally activated. One has homology to NADH-ubiquinone oxidoreductase chain 4 protein, and is also probably changed as a result of the detransforming process. Another is homologous to a human sequence which encodes a 27 kDa protein, p27(BBP/eIF6), that is involved in the biogenesis of 60S ribosomal subunit, and in cell lines of epithelial origin binds to beta integrin. This has not previously been described as transformation-related, and could have a causative role in reverse transformation. The third has homology, with transcriptional or processing variations, to a human genomic sequence, a positional candidate for a tumour suppressor gene, encoding the Krit1 protein which interacts with the Ras-family GTPase Krev-1.
机译：CHO-K1和其他细胞的化学逆向转换是一个公认的现象，在这种现象中，对环状AMP和其他药物的响应，致癌转化的细胞重新获得了成纤维细胞形态，接触抑制和锚定依赖性生长。已经证明基因转录和酶活性的有限变化与这些形态和生理变化一致。我们已经使用了部分差异显示来鉴定在反向转化中被转录调节的四个基因。其中之一是编码核糖体蛋白S18的，可能是去转化过程的结果，其转录受到抑制。另外三个被转录激活。一个与NADH-泛醌氧化还原酶链4蛋白具有同源性，并且也可能由于去转化过程而改变。另一个与编码27 kDa蛋白p27（BBP / eIF6）的人序列同源，该蛋白与60S核糖体亚基的生物发生有关，并且在上皮起源的细胞系中与β整联蛋白结合。以前没有将其描述为与转换有关，并且可能在反向转换中起因果作用。第三个与人类基因组序列具有同源性，具有转录或加工变异性，是人类抑癌基因的位置候选物，编码与Ras家族GTPase Krev-1相互作用的Krit1蛋白。

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