Vilette D, Emanoil-Ravier R, Buffe D, Rimbaut C, Peries J
Cancer Res. 1987 Feb 1;47(3):867-73.
Embryonal carcinoma (EC) cells are malignant components of murine teratoma tumors. To extend our earlier findings concerning c-Ki-ras amplification in the embryonal carcinoma PCC4 cell line, we examined the c-Ki-ras protooncogene and its expression in other EC cell lines. We report here that c-Ki-ras amplification is not a general feature of EC cell lines since neither PCC3, PCC6, nor F9 cell lines have an amplified copy number of this protooncogene. Furthermore, molecular analysis of three independently passaged PCC4 cell lines showed marked heterogeneity for c-Ki-ras amplification. Two PCC4 cell lines showed amplified copy number and elevated expression of c-Ki-ras whereas the original one does not, suggesting that this gene amplification occurred through laboratory passage. Malignancy in syngeneic mice of PCC4 with or without an amplified c-Ki-ras gene was also examined. Our results indicate that c-Ki-ras amplification alone is not a determining factor in the malignant behavior of EC cells.
胚胎癌（EC）细胞是鼠畸胎瘤肿瘤的恶性成分。为了扩展我们早期关于胚胎癌PCC4细胞系中c-Ki-ras基因扩增的研究结果，我们检测了c-Ki-ras原癌基因及其在其他EC细胞系中的表达。我们在此报告，c-Ki-ras基因扩增并非EC细胞系的普遍特征，因为PCC3、PCC6和F9细胞系均没有该原癌基因的扩增拷贝数。此外，对三个独立传代的PCC4细胞系进行的分子分析显示，c-Ki-ras基因扩增存在显著异质性。两个PCC4细胞系显示出c-Ki-ras基因的扩增拷贝数及表达升高，而原始细胞系则不然，这表明该基因扩增是在实验室传代过程中发生的。我们还检测了具有或不具有扩增的c-Ki-ras基因的PCC4细胞在同基因小鼠中的致瘤性。我们的结果表明，单独的c-Ki-ras基因扩增并非EC细胞恶性行为的决定性因素。
