These effects were linked to downregulation of EMT markers such as β-catenin, N-cadherin, TGF-β, and Twist1, while E-cadherin levels remained stable, indicating preserved epithelial characteristics and inhibition of mesenchymal transition (Lee et al., 2014); this is supported by CHR’s reducing impact on the EMT status of breast cancer cells (Yang et al., 2014). This evidence concerns the gene TWIST1 and breast cancer.