SMAD7 and breast cancer: Using breast cancer cell lines derived from a common genetic background (i.e., MCF10A) which accumulated distinct genetic/epigenetic alterations in vivo thus acquiring properties associated with gradual progression from nontumorigenic to carcinogenic state, these authors showed that Smad7 overexpression suppresses migration and invasion of mesenchymal-like MCF10CA1h cells, a malignant variant of Ras-transformed MCF10A cells, by reversing the DNA methylation status of specific epithelial markers (i.e., E-cadherin, γ-catenin, and β-catenin) thus inducing their re-expression [58].