THE REGULATORY MECHANISM OF ONCOGENE EXPRESSION

尽管有相当多的资料， 逆转录病毒癌基因及其特异蛋白的分子结构 对于这些产品，人们对其转化机制知之甚少 细胞 此外，原癌基因，逆转录病毒的细胞对应物， 在正常细胞中发现了癌基因，但它们的表达很低， 这种低表达的机制尚不清楚。 可以想象 增加肿瘤发展的物质， 细胞增殖是通过改变细胞的数量或时间来实现的。 细胞癌基因的表达。 了解细胞机制 控制病毒和细胞癌基因的表达， 因此，提供了一个深入了解肿瘤细胞生长的机制， 和肿瘤的发展。 偶尔，肿瘤细胞分化 然后完全退化。 有人认为cAMP 可能与肿瘤细胞的形态分化有关 由于用二丁酰cAMP、前列腺素E1 和cAMP-磷酸二酯酶抑制剂诱导不可逆的形态学 分化 这种分化可能是 恶性肿瘤的支持是观察到没有肿瘤产生时， 将这些处理过的细胞接种到动物体内。 研究影响转化的表型逆转的因素， 细胞，我们选择了NIH 3 T3细胞的细胞系433，其含有 转化Ha-MuSV的ras基因，侧接MMTV的LTR和克隆13-3B-4 的NIH 3 T3细胞，Ha-MuSV DNA转染子。 我们也用人类癌症 细胞系 本研究的目的是调查 细胞内调节因子，如环核苷酸、激素和 生长因子对ras基因表达的影响。

In spite of the relatively large body of information concerning the molecular structure of retrovirus oncogenes and their specific protein products, little is known about the mechanisms by which they transform cells. Moreover, proto-oncogenes, the cellular counterpart of retroviral oncogenes, have been found in normal cells but their expression is low and the mechanism for this low expression is not known. It is conceivable that substances that increase tumor development by apparently increasing cellular proliferation do so by altering the quantitative or temporal expression of cellular oncogenes. Understanding the cellular mechanisms governing the expression of both viral and cellular oncogenes would therefore provide an insight into the mechanism of neoplastic cell growth and tumor development. Occasionally, tumor cells differentiate spontaneously and then regress completely. It has been suggested that cAMP may be linked with the morphological differentiation of neoplastic cells since treatment of some tumor cells with dibutyryl cAMP, prostaglandin E1 and inhibitors of cAMP-phosphodiesterase induces irreversible morphological differentiation. That this differentiation may be a reversion of malignancy is supported by the observation that no tumor is produced when these treated cells are inoculated into animals. To investigate factors that affect phenotypic reversion of transformed cells, we have chosen a cell line 433 of NIH 3T3 cells containing the transforming ras gene of Ha-MuSV flanked by LTR of MMTV and clone 13-3B-4 of NIH 3T3 cells, the Ha-MuSV DNA transfectant. We also used human cancer cell lines. The goal of this study is to investigate the effect of intracellular regulatory factors, such as cyclic nucleotides, hormones, and growth factors on the expression of ras gene.