The v‐mos and H‐ras oncogene expression represses glucocorticoid hormone‐dependent transcription from the mouse mammary tumor virus LTR.
The v‐mos and H‐ras oncogene expression represses glucocorticoid hormone‐dependent transcription from the mouse mammary tumor virus LTR.
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v-mos 和 H-ras 癌基因表达抑制小鼠乳腺肿瘤病毒 LTR 的糖皮质激素依赖性转录。
DOI：
10.1002/j.1460-2075.1986.tb04541.x
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发表时间：
1986
期刊：
影响因子：
--
通讯作者：
B. Groner
中科院分区：
文献类型：
--
作者：
R. Jaggi;Brian Salmons;D. Muellener;B. Groner
我们通过与小鼠乳腺肿瘤病毒长末端重复序列（MMTV LTR）的启动子区域体外重组并转染到NIH 3T3细胞中，使病毒mos癌基因（v-mos）、激活的人H-ras癌基因[H-ras（A）]和正常人H-ras原癌基因[H-ras（N）]受到糖皮质激素的转录调节。选择表现出严格依赖于生长培养基中激素的存在的转化表型的细胞克隆。在转录率、mRNA和蛋白质积累水平上研究了嵌合基因的表达作为激素刺激后时间的函数。添加激素后，癌基因表达迅速达到高水平，但在激素持续存在下下降。对 LTR v-mos 和 LTR H-ras (A) 转染细胞的细胞核转录率的测量显示，在激素初始刺激后，LTR v-mos 和 LTR H-ras (A) 转录受到抑制。 LTR H-ras (N) 转录不受影响。含有 LTR v-mos 或 LTR H-ras (A) 的细胞中独立转染的 LTR H-2Ld 构建体也受到转录抑制。这些实验证明了癌基因产物对糖皮质激素依赖性 MMTV LTR 转录的转录抑制作用。
We have subjected the viral mos oncogene (v‐mos), the activated human H‐ras oncogene [H‐ras (A)] and the normal human H‐ras protooncogene [H‐ras (N)] to the transcriptional regulation of glucocorticoid hormones by in vitro recombination with the promoter region of the mouse mammary tumor virus long terminal repeat (MMTV LTR) and transfection into NIH 3T3 cells. Cell clones were selected which exhibit a transformed phenotype strictly dependent on the presence of hormone in the growth medium. The expression of the chimeric genes as a function of time after hormone stimulation was studied at the level of transcriptional rate, mRNA and protein accumulation. Oncogene expression was stimulated rapidly to high levels, after hormone addition, but declined in the continuous presence of hormone. Measurements of the transcriptional rates in nuclei from LTR v‐mos and LTR H‐ras (A) transfected cells showed a repression of LTR v‐mos and LTR H‐ras (A) transcription after the initial stimulation by hormone. LTR H‐ras (N) transcription was not affected. An independently transfected LTR H‐2Ld construct in LTR v‐mos or LTR H‐ras (A) containing cells is also transcriptionally repressed. These experiments demonstrated a transcriptional repression effect of the oncogene products on the glucocorticoid hormone‐dependent MMTV LTR transcription.