作为钙粘附蛋白家族成员之一，cadherin 11在胚胎发育，组织形成，神经元生长及肿瘤转移等方面都起着非常重要的作用。研究发现，cadherin 11的表达对多种肿瘤细胞的转移有着明显的促进作用。然而，调控cadherin 11转录表达的分子机制，目前还不了解。在我们以前的研究中，我们报道了HOXC8蛋白的表达明显地增强了乳腺癌细胞的转移。最近我们的预实验结果显示，在乳腺癌细胞中HOXC8是cadherin 11的转录因子之一，ILF3与HOXC8相互作用，且有可能参与了HOXC8对cadherin 11的转录调控。本研究拟鉴定在乳腺癌细胞中HOXC8对cadherin 11转录的调控机制，包括鉴定ILF3和其它蛋白因子协同参与HOXC8对cadherin 11的转录调控。本项目是一个创新的科研计划，将首次阐明cadherin 11转录的调控机制，为抑制乳腺癌的转移提供新的作用靶点。

As a member of cadherin family, cadherin 11 plays important roles in embryo development, tissue morphogenesis, neuron growth and cancer metastasis, etc. It has been reported that cadherin 11 expression is associated with increased metastasis in several cancers. However, very little is known about the regulation of cadherin transcription. In our previous study, we reported that HOXC8 protein expression significantly enhanced breast cancer cell metastasis. Recently our preliminary data show that HOXC8 functions as a transcription factor in regulation of cadherin 11 transcription in breast cancer cells, and ILF3 (interleukin enhancer-binding factor 3) interacts with HOXC8 and is probably involved in cadherin 11 transcription regulation, too. This study will determine how HOXC8 regulates cadherin 11 transcription in breast cancer cells, and further identify ILF3 and other protein co-factors that are involved in HOXC8-regulated cadherin 11 transcription. This proposal is an innovate scientific research plan, and will be the first one to elucidate the mechanism of cadherin 11 transcription regulation in breast cancer cells, which will provide novel anti-metastasis therapeutic target sites for breast cancer.