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nature portfolio recent research shows privacy policy cancer research nature hela cdna library editing advertising social media 0/ reprints confer csc-related traits speckle-type poz protein pkcepsilon-dependent mechanism snail-mediated e-cadherin repression genome chip-chip analysis twist-expressing t47d cells gsk-3beta-mediated phosphorylation full size image twist-t47d cells compared undergone twist-mediated emt providing ctgf-luc plasmid inflammation-induced cell migration twist-overexpressing t47d cells g-protein-coupled receptors par1/gα13 binding conformation t47d-twist cell types normal breast epithelia twist-mediated par1 induction mesenchymal marker n-cadherin epithelial marker e-cadherin subsequently activates yap/taz confers tumor cells epithelial-mesenchymal transition epithelial–mesenchymal transition national cancer institute-frederick cellular de-differentiation program matrigel-coated boyden chambers high-gain sensors breast cancer progression stem cell traits human breast cancer permissions real-time pcr luciferase reporter assay mammary epithelial cells twist promotes induction twist-expression affects proliferation cancer stem cell twist-expressing t47d stable cell line

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         description:Twist is a key transcription factor for Epithelial-mesenchymal transition (EMT), which is a cellular de-differentiation program that promotes invasion and metastasis, confers tumor cells with cancer stem cell (CSC)-like characteristics and increases therapeutic resistance. However, the mechanisms that facilitate the functions of Twist remain unclear. Here we report that Twist overexpression increased expression of PAR1, an upstream regulator of the Hippo pathway; PAR1 promotes invasion, migration and CSC-like properties in breast cancer by activating the transcriptional co-activator TAZ. Our study indicates that Hippo pathway inhibition is required for the increased migratory and invasiveness ability of breast cancer cells in Twist-mediated EMT.
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