STUDIES ON THE ACTIVATION OF ONCOGENES IN VIRUSES AND HUMAN TUMORS

我们已经分析了ovc癌基因的一部分的DNA序列， 在DNA转染期间激活的人转化序列， 来源于人卵巢癌细胞系OVCAR-3。 将该序列与GenBank中包含的序列进行比较 数据库显示没有显著的同源性，这表明， 与以前的杂交数据一致，OVC代表了一种 ?以前未发现的人类癌基因。 poly-A+ RNA分析 从几个正常的和转化的人类细胞系表明， ovc序列在OVCAR-3亲本细胞系中表达， 其他三种人类腺癌 我们之前已经证明用抗氧化剂处理小鼠成纤维细胞 衣霉素是一种糖基化抑制剂， RD 114猫内源性病毒及其假型的感染。 我们现在已经证明了其他几种糖基化抑制剂， 其作用于沿着糖基化途径的不同点，还 也有类似的效果。 此外，小鼠淋巴细胞表现出 与衣霉素相似的特性。 这表明 这可能代表小鼠细胞的共同特征。 我们已经测试了来自两个细胞系的细胞DNA的能力， 来自甲基胆蒽诱导的小鼠纤维肉瘤（TN-10），和 它们表现出不同的转移潜能， 细胞 在高浓度转染后诱导病灶。 效率，转化细胞已经获得了 在没有血清或蛋白质生长因子的情况下生长。 没有 检测到几种特征明确的癌基因的重排， 在转染细胞中，但病灶似乎含有扩增的拷贝 小鼠K-ras癌基因的表达。

We have analyzed the DNA sequence of a portion of the ovc oncogene, a human transforming sequence activated during DNA transfection and derived from the human ovarian carcinoma cell line, OVCAR-3. Comparison of this sequence with sequences contained in the GenBank data base reveals no significant homologies, suggesting that, consistent with previous hybridization data, ovc represents a ?previously unidentified human oncogene. Analysis of poly-A+ RNA from several normal and transformed human cell lines indicates that ovc sequences are expressed in the OVCAR-3 parent cell line and three other human adenocarcinomas. We had previously shown that treatment of mouse fibroblasts with tunicamycin, a glycosylation inhibitor, renders them susceptible to infection by RD114 cat endogenous virus and its pseudotypes. We have now shown that several other inhibitors of glycosylation, which act at different points along the glycosylation pathway, also have a similar effect. In addition, mouse lymphoid cells exhibit similar properties when exposed to tunicamycin. This suggests that this may represent a common feature of mouse cells. We have tested the ability of cell DNA from two cell lines derived from a methylcholanthrene-induced mouse fibrosarcoma (TN-10), and which exhibit differing metastatic potentials, to transform NIH 3T3 cells. Foci are induced following transfection at high efficiencies, and transformed cells have acquired the ability to grow in the absence of serum or protein growth factors. No rearrangements of several well-characterized oncogenes are detected in transfected cells, but foci appear to contain amplified copies of the murine K-ras oncogene.