Modulation by retinoids of mRNA levels for nuclear retinoic acid receptors in murine melanoma cells.
Modulation by retinoids of mRNA levels for nuclear retinoic acid receptors in murine melanoma cells.
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类视黄醇对小鼠黑色素瘤细胞核视黄酸受体 mRNA 水平的调节。
作者：
J. Clifford;M. Petkovich;P. Chambon;R. Lotan
维甲酸对小鼠S91-C2黑色素瘤细胞的生长抑制和分化促进作用基因表达的特定改变是这些效应的合理机制。由于核视黄酸受体（RAR）可能是类维生素A诱导的基因表达变化的介质，我们使用北方印迹法分析S91-C2细胞中RAR α、RAR β和RAR γ的表达。10（-7）和10（-6）M β-全反式维甲酸（RA）处理24 h后，RAR α和RAR γ mRNA表达增加1.5 - 2倍，而低浓度RA则无效。在未处理细胞中检测不到RAR β mRNA，在低至10（-9）M的RA浓度处理24小时后检测到RAR β mRNA，并且其水平随着高达10（-6）M的RA而增加。在后一种剂量下，RAR β mRNA诱导在4小时发生，并逐渐增加，在处理24小时后达到平台。RAR β mRNA的诱导在4小时不抑制放线菌酮在抑制蛋白质合成的浓度超过90%。几种类维生素A和相关的合成化合物，包括13-顺式RA、TTNPB、Ch55、Am80和RA的三氟甲基壬氧基苯基类似物，也能诱导RAR β mRNA，而用10（-6）M视黄醇、TTNP（TTNPB的脱羧类似物）或RA的苯基类似物处理24小时则不能诱导RAR β mRNA。除了视黄醇和RA的三氟甲基壬氧基苯基类似物外，类维生素A诱导RAR β mRNA的能力与其生长抑制作用相关。然而，来自S91-C2细胞的RA抗性突变体亚克隆S91-C154显示RA对RAR α和RAR γ的mRNA水平以及RA对RAR β的诱导与敏感的S91-C2细胞中检测到的相似。与S91黑色素瘤细胞一样，另外两种小鼠黑色素瘤细胞系K-1735 P和B16-F1组成型表达RAR α和RAR γ mRNA。RA仅在B16-F1细胞中增加RAR β mRNA的水平，尽管两者的生长均被RA抑制。这些结果表明，RA可以直接且快速地诱导某些小鼠黑色素瘤细胞中高亲和力核受体mRNA的表达，但这种诱导不足以抑制生长。
Retinoids inhibit the growth and enhance the differentiation of murine S91-C2 melanoma cells. Specific alterations in gene expression are a plausible mechanism for these effects. Since nuclear retinoic acid receptors (RAR) are likely mediators of retinoid-induced changes in gene expression, we used Northern blotting to analyze the expression of RAR alpha, RAR beta, and RAR gamma in S91-C2 cells. mRNA for both RAR alpha and RAR gamma was detected in these cells, but no RAR beta mRNA could be found. Treatment with 10(-7) and 10(-6) M beta-all-trans-retinoic acid (RA) for 24 h caused a 1.5- to 2-fold increase in RAR alpha and RAR gamma mRNA, whereas lower concentrations of RA were ineffective. RAR beta mRNA, which was undetectable in untreated cells, was detected after 24 h of treatment with a RA concentration as low as 10(-9) M, and its level increased with up to 10(-6) M RA. At the latter dose, RAR beta mRNA induction occurred by 4 h and increased progressively, reaching a plateau after 24 h of treatment. RAR beta mRNA induction at 4 h was not inhibited by cycloheximide at a concentration that suppressed protein synthesis by more than 90%. Several retinoids and related synthetic compounds, including 13-cis RA, TTNPB, Ch55, Am80, and the trifluoromethyl nonyloxyphenyl analog of RA, also induced RAR beta mRNA, whereas a 24-h treatment with 10(-6) M retinol, TTNP (a decarboxylated analog of TTNPB), or the phenyl analog of RA failed to induce RAR beta mRNA. With the exception of retinol and the trifluoromethyl nonyloxyphenyl analog of RA, the ability of the retinoids to induce RAR beta mRNA and their growth inhibitory effect were correlated. However, S91-C154, a RA-resistant mutant subclone derived from S91-C2 cells, showed mRNA levels of RAR alpha and RAR gamma and induction of RAR beta by RA similar to those detected in the sensitive S91-C2 cells. Like the S91 melanoma cells, two other mouse melanoma cell lines, K-1735P and B16-F1, constitutively expressed RAR alpha and RAR gamma mRNAs. The level of RAR beta mRNA was increased by RA only in B16-F1 cells, although the growth of both was inhibited by RA. These results demonstrate that RA can, directly and rapidly, induce the expression of mRNA for a high affinity nuclear receptor in some murine melanoma cells and that this induction is not sufficient to inhibit growth.
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视黄酸和表皮生长因子对表皮生长因子受体基因表达的调节。
DOI：
--
发表时间：
1989
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Thompson,KL;Rosner,MR
通讯作者：
Rosner,MR
DOI：
--
发表时间：
1988
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Chiocca,EA;Davies,PJ;Stein,JP
通讯作者：
Stein,JP
DOI：
10.1073/pnas.85.2.329
发表时间：
1988
影响因子：
11.1
作者：
G. Larosa;L. Gudas
通讯作者：
G. Larosa;L. Gudas
视黄酸选择性刺激大鼠垂体细胞中的生长激素分泌和信使核糖核酸水平。
影响因子：
4.8
作者：
Morita,S;Fernandez-Mejia,C;Melmed,S
通讯作者：
Melmed,S
糖皮质激素对培养的骨髓瘤细胞的影响：生长抑制与糖皮质激素受体信使 RNA 诱导的相关性。
影响因子：
11.2
作者：
Gomi,M;Moriwaki,K;Katagiri,S;Kurata,Y;Thompson,EB
通讯作者：
Thompson,EB