Upregulation of TCF4 expression as a transcriptional target of β-catenin/p300 complexes during trans-differentiation of endometrial carcinoma cells
Upregulation of TCF4 expression as a transcriptional target of β-catenin/p300 complexes during trans-differentiation of endometrial carcinoma cells
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DOI：
10.1038/labinvest.3700273
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发表时间：
2005-06-01
影响因子：
5
通讯作者：
Okayasu, I
中科院分区：
文献类型：
--
作者：
Saegusa, M;Hashimura, M;Okayasu, I
β-catenin的核稳定化及其与TCF/LEF因子的相互作用是Wnt/β-catenin信号通路转导的关键事件。我们以前的研究表明，细胞核β-连环蛋白的积累提供了一个初始信号，转分化向鳞状细胞表型的子宫内膜癌（Em Ca）细胞在TCF 4依赖的方式，这使得这一可能的因素，积极的预后。然而，很少有人知道TCF 4在Em Cas中的表达调控。我们发现β-连环蛋白可以直接诱导TCF 4启动子的转录，p300辅激活因子可以增强这种作用。在临床病例中，发现细胞核中β-catenin积聚与桑椹胚和周围腺癌病灶中TCF 4免疫反应经常重叠，显示出显著的正相关性（r = 0.82，P
Nuclear stabilization of beta-catenin and its interaction with TCF/LEF factors are key events in transduction of the Wnt/beta-catenin signal pathway. Our previous study indicated that nuclear beta-catenin accumulation provides an initial signal for trans-differentiation toward the squamoid phenotype of endometrial carcinoma (Em Ca) cells in a TCF4-dependent manner, which makes this a possible factor for a positive prognosis. However, little is known about regulation of TCF4 expression in Em Cas. We show here that beta-catenin can directly induce transcription from the TCF4 promoter, the effect being enhanced by the p300 coactivator. In clinical cases, nuclear beta-catenin accumulation was found to frequently overlap with TCF4 immunoreactivity in morules and surrounding glandular carcinoma lesions, showing a significant positive correlation (r = 0.82, P