Global gene expression profiles associated with retinoic acid-induced differentiation of embryonal carcinoma cells
Global gene expression profiles associated with retinoic acid-induced differentiation of embryonal carcinoma cells
复制标题
与维甲酸诱导胚胎癌细胞分化有关的全基因表达谱
DOI：
10.1002/mrd.20444
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发表时间：
2006-07-01
影响因子：
2.5
通讯作者：
McCormick, Paulette J.
中科院分区：
文献类型：
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作者：
Eifert, Cheryl;Sangster-Guity, Niquiche;McCormick, Paulette J.
我们已经评估了视黄酸（RA）治疗F9胚胎癌（EC）细胞，诱导分化成原始内胚层，基因表达模式的影响。将F9细胞暴露于培养物中的RA，并在暴露后的早期（8小时）和后期（24小时）用基于cDNA的微阵列检查全局表达模式。在检测的1,176个已知转录物中，我们确定了57个基因（4.8%）在8和/或24小时对RA有反应：35个被诱导，20个被抑制，2个在这些时间点被差异调节。为了确定我们的结果是否依赖于所采用的阵列技术，我们还评估了24小时时基于微阵列的RA反应。通过这些更密集的阵列（12，488个基因），我们确定了另外353个RA调节基因（2.8%）：173个上调，180个下调。因此，共鉴定出410个受RA调控的基因，诱导或抑制的基因数量大致相等。尽管在两个阵列平台上发现的许多基因的表达是一致的，但一些基因的结果是不同的。对这些基因的一个子集的定量PCR研究支持用cDNA阵列获得的结果。我们的研究结果证实了几个已知的RA反应基因的调控，我们还确定了一些基因以前不知道是RA反应。被诱导的这些新基因可能有助于从增殖向分化转变所需的细胞过程，而那些下调的新基因可能有助于维持细胞增殖。
We have evaluated the effects of retinoic acid (RA) treatment of F9 embryonal carcinoma (EC) cells, which induces differentiation into primitive endoderm, on gene expression patterns. F9 cells were exposed to RA in culture, and global expression patterns were examined with cDNA-based microarrays at early (8 hr) and later times (24 hr) after exposure. Of the 1,176 known transcripts examined, we identified 57 genes (4.8%) that were responsive to RA at 8 and/or 24 hr: 35 were induced, 20 were repressed, and 2 were differentially regulated at these time points. To determine if our results were dependent on the array technology employed, we also evaluated the response to RA at 24 hr with oligonucleoticle-based arrays. With these more dense arrays (12,488 genes), we identified an additional 353 RA-regulated genes (2.8%): 173 were upregulated and 180 were down-regulated. Thus, a total of 410 genes regulated by RA were identified with roughly equivalent numbers induced or repressed. Although the expression of many genes found on both array platforms was consistent, the results for some genes were disparate. Quantitative PCR studies on a subset of these genes supported the results obtained with the cDNA arrays. Our results confirmed the regulation of several known RA-responsive genes and we also identified a number of genes not previously known to be RA-responsive. Those novel genes that were induced presumably contribute to the cellular processes required for a shift from proliferation to differentiation, whereas those new genes that were down-regulated may possibly contribute to the maintenance of cell proliferation.