Sox4 functions as a positive regulator of beta-catenin signaling through upregulation of TCF4 during morular differentiation of endometrial carcinomas

在子宫内膜癌（EmCa）细胞中，Sox4可以通过在转录水平上调TCF4来增强β -catenin/TCF4的转录，而与β -catenin无直接关联。稳定过表达Sox4的细胞增殖率显著降低，p21waf1表达增加，而低表达Sox4的细胞生长增加。Sox7可以通过转录上调Sox4的表达。最后，Sox4的免疫反应性在Em Cas的小分子中经常被发现，其表达与β -catenin、TCF4和Sox7的状态呈正相关，与细胞增殖呈负相关。因此，这些数据表明，Sox4可能在Em - Ca细胞的结节分化过程中通过改变TCF4的表达，作为β -catenin信号的正调节因子，从而抑制细胞增殖。

In endometrial carcinoma (EmCa) cells, Sox4 could enhance beta-catenin/TCF4 transcription, through up-regulation of TCF4 at the transcription level, without any direct beta-catenin association. Cells stably overexpressing Sox4 showed significant decreases in proliferation rate, along with increases in expression of p21waf1, in contrast to increased cell growth observed with knockdown. Sox7 could transcriptionally up-regulate Sox4 expression. Finally, Sox4 immunoreactivity was frequently pronounced in morules of Em Cas, the expression being positively correlated with status of beta-catenin, TCF4, and Sox7, and inversely with cell proliferation. These data therefore suggest that Sox4 may serve as a positive regulator of beta-catenin signaling through alteration in TCF4 expression during morular differentiation of Em Ca cells, leading to inhibition of cell proliferation.