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首页> 外文期刊>Molecular and Cellular Biology >Genome-Wide Pattern of TCF7L2/TCF4 Chromatin Occupancy in Colorectal Cancer Cells
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Genome-Wide Pattern of TCF7L2/TCF4 Chromatin Occupancy in Colorectal Cancer Cells

机译：大肠癌细胞中TCF7L2 / TCF4染色质占用的全基因组模式

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Wnt signaling activates gene expression through the induced formation of complexes between DNA-binding T-cell factors (TCFs) and the transcriptional coactivator β-catenin. In colorectal cancer, activating Wnt pathway mutations transform epithelial cells through the inappropriate activation of a TCF7L2/TCF4 target gene program. Through a DNA array-based genome-wide analysis of TCF4 chromatin occupancy, we have identified 6,868 high-confidence TCF4-binding sites in the LS174T colorectal cancer cell line. Most TCF4-binding sites are located at large distances from transcription start sites, while target genes are frequently “decorated” by multiple binding sites. Motif discovery algorithms define the in vivo-occupied TCF4-binding site as evolutionarily conserved A-C/G-A/T-T-C-A-A-A-G motifs. The TCF4-binding regions significantly correlate with Wnt-responsive gene expression profiles derived from primary human adenomas and often behave as β-catenin/TCF4-dependent enhancers in transient reporter assays.
机译：Wnt信号传导通过诱导DNA结合T细胞因子（TCF）与转录共激活因子β-catenin之间复合物的诱导而激活基因表达。在结直肠癌中，激活的Wnt途径突变通过TCF7L2 / TCF4目标基因程序的不适当激活而转化上皮细胞。通过基于DNA阵列的TCF4染色质占用的全基因组分析，我们在LS174T大肠癌细胞系中确定了6,868个高可信度TCF4结合位点。大多数TCF4结合位点与转录起始位点相距很远，而靶基因经常被多个结合位点“修饰”。主题发现算法将体内占据的TCF4结合位点定义为进化保守的A-C / G-A / T-T-C-A-A-A-G主题。 TCF4结合区与源自原发性人腺瘤的Wnt响应基因表达谱显着相关，并且在瞬时报告基因测定中通常充当β-catenin/ TCF4依赖性增强子。

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