In human breast cancer cells, HGF downregulates TJ molecules (e.g., claudin-1) to promote epithelial–mesenchymal transition [35], while in endothelial monolayers, it reduces transendothelial resistance by inducing tyrosine phosphorylation of occludin and ZO-1, a post-translational modification known to weaken TJ stability [36]. This evidence concerns the gene TJP1 and breast carcinoma.