Growth control in mouse Y-1 adrenocortical tumor cells: role of c-Ki-ras amplification and effects of ACTH.

E Kimura, H A Armelin
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Abstract

Even though the proto-oncogene c-Ki-ras is found to be amplified and overexpressed in the malignant Y-1 mouse corticoadrenal cell line, evidence for a causal relationship between c-Ki-ras overexpression and malignancy is still lacking. Such evidence is presented in this report. Amplified c-Ki-ras was found in both sublines of Y-1 cells that carry DM (double minute) or HSR (homogeneously stained region) chromosomes. Y-1 normal revertants did not display c-Ki-ras amplified sequences. Spontaneous retransformation of the normal revertants yielded anchorage-independent non-tumorigenic cells in which c-Ki-ras was not amplified. We propose that c-Ki-ras amplification is required to maintain the malignant state of Y-1 cells. Constitutive expression of poly A RNA homologous to viral sequences were detected in all sublines of Y-1 cells (malignant or normal revertants) by Northern hybridization using probes derived from the pFBJ-2 provirus. Rapid induction of c-fos proto-oncogene mRNA and late reduction in the levels of poly A+ viral transcripts resulted from ACTH treatment of Y-1 cells. However, ACTH treatment did not change c-Ki-ras mRNA levels.

小鼠Y-1肾上腺皮质肿瘤细胞的生长控制:c-Ki-ras扩增的作用和ACTH的影响。
尽管发现原癌基因c-Ki-ras在恶性Y-1小鼠皮质肾上腺细胞系中被扩增和过表达,但c-Ki-ras过表达与恶性肿瘤之间的因果关系仍然缺乏证据。本报告提出了这些证据。在携带DM(双分钟)或HSR(均匀染色区)染色体的Y-1细胞的两个亚系中都发现了扩增的c-Ki-ras。Y-1正常复归物不显示c-Ki-ras扩增序列。正常复归物的自发再转化产生不依赖于锚定的非致瘤性细胞,其中c-Ki-ras不扩增。我们认为维持Y-1细胞的恶性状态需要c-Ki-ras扩增。利用来自pFBJ-2原病毒的探针进行Northern杂交,在Y-1细胞的所有亚系(恶性或正常逆转录细胞)中检测到与病毒序列同源的聚A RNA的组成性表达。ACTH处理Y-1细胞导致c-fos原癌基因mRNA的快速诱导和poly A+病毒转录物水平的晚期降低。然而,ACTH治疗未改变c-Ki-ras mRNA水平。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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