DACH1 inhibits SNAI1-mediated epithelial-mesenchymal transition and represses breast carcinoma metastasis.

摘要: Epithelial-mesenchymal transition (EMT) has a major role in cancer progression and metastasis. However, the specific mechanism of transcriptional repression involved this process remains largely unknown. Dachshund homologue 1 (DACH1) expression is lost invasive breast with poor prognosis, DACH1 regulating metastasis poorly understood. In study, significant correlation between morphology cells was observed. Subsequent investigation into relationship EMT showed that overexpression ZR-75-30 induced shift towards epithelial cell-cell adhesion, as well increased marker E-cadherin suppressed cell migration invasion. contrast, silencing MCF-7 T47D disrupted contact, reduced E-cadherin, also specifically interacted SNAI1, but not SNAI2, to form complex, which could bind E-box on promoter an SNAI1-dependent manner. inhibited activity leading activation cells. Furthermore, level correlated extent mouse model. significantly decreased growth 4T1/Luc BALB/c mice. Analysis tissue samples taken from human cancers SNAI1-positive cancer. Collectively, our data identified new mechanistic pathway for regulation cells, one based by direct DACH1-SNAI1 interaction.