TGF-beta and epithelial-to-mesenchymal transitions.

By Jiri Zavadil, Erwin P. Bottinger. Oncogene, 2005

931 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/ceae82b08d903975bbecc46115d41a202cecfcf3

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Citations in the corpus

Transcriptional regulation of cell polarity in EMT and cancer (2008, background): “TGF-b is one of the more robust cues inducing EMT in different model systems (reviewed by Zavadil and Bottinger, 2005), leading to the upregulation of several EMT inducers, including SNAI1/SNAI2, ZEB1, Twist and the Id factors through Smad-dependent and Smad-independent pathways (Peinado et al.,…”
LSD1 is a subunit of the NuRD complex and targets the metastasis programs in breast cancer. (2009, background): “(C) Inhibition of TGFb1 signaling by SB-431542 suppressed the invasionpromoting effect of LSD1 knockdown.”
Inflammation and EMT: an alliance towards organ fibrosis and cancer progression (2009, background): “…above, TGF-b1 contributes to the formation of myofibroblasts through the activation of resident fibroblasts and by inducing the transition to mesenchyme of epithelial and endothelial cells via EMT or EndMT, respectively (Zavadil & Böttinger, 2005; Zeisberg & Kalluri, 2008; Zeisberg et al, 2008).”
The epithelial–mesenchymal transition: new insights in signaling, development, and disease (2006, unknown): “in signaling, development, and disease”
Dynamic EMT: a multi‐tool for tumor progression (2021, unknown): “…a TEAD/YAP/AP 1 ternary complex to regulate activity of distal enhancers, whereas ZEB 1 and YAP are part of a multimeric complex with AP 1 factors independent of direct ZEB 1 DNA binding to drive gene expression on a genome-wide level (Zanconato et al , 2015 ; Feldker et al , 2020 ) (Fig 4 B).”
EMT subtype influences epithelial plasticity and mode of cell migration (2018, background): “TGFβ treatment induces a C-EMT phenotype EMT is often induced experimentally by exposing cultured cells to exogenous growth factors – most commonly TGFβ – resulting in the downregulation of transcripts for Ecad and other epithelial genes across a variety of tumor types (Zavadil and Bottinger, 2005).”