Downregulation of caveolin-1 function by EGF leads to the loss of E-cadherin, increased transcriptional activity of beta-catenin, and enhanced tumor cell invasion.

By Zhimin Lu, Sourav Ghosh, Zhiyong Wang, T. Hunter. Cancer Cell, 2003

673 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/d0a1a101a7afd94f0518b6312358dcaba18eaf96

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Citations in the corpus

Dynamic EMT: a multi‐tool for tumor progression (2021, positive): “EGF induces EMT by upregulation of SNAI 1 , TWIST 1 and ZEB 1 in different cell lines through MAPK/ERK as well as JNK/STAT 3 activation (Lu et al , 2003 ).”
Epithelial-mesenchymal transitions in development and disease. (2009, background): “EGF is known to induce EMT by promoting E-cadherin endocytosis (Lu et al., 2003), but it can also induce the expression of both Snail and Twist, repressing E-cadherin transcription among other targets (Lee et al., 2008; Lo et al., 2007).”
The Snail genes as inducers of cell movement and survival: implications in development and cancer (2005, background): “It reduces E-Cadherin function by promoting its caveolin-dependent endocytosis, which leads to subsequent Snail induction and to the triggering of EMT (Lu et al., 2003).”
Clathrin- and non-clathrin-mediated endocytic regulation of cell signalling (2005, background): “Furthermore, a recent report indicates that EGF stimulates the caveolin-dependent internalization of E-cadherin, which is consistent with the idea that the activity of this pathway is regulate”
Epithelial—mesenchymal and mesenchymal—epithelial transitions in carcinoma progression (2007, background): “Decreased E-cadherin expression is correlated with various indices of prostate cancer progression including grade, local invasiveness, dissemination into the blood, and tumor relapse after radiotherapy (Loric et al., 2001; Mason et al., 2002; Ray et al., 2006).”
The Role of Snail in EMT and Tumorigenesis (2013, background): “For example, receptor tyrosine kinases (RTKs) signaling, activated by HGF, FGF, or EGF, acts through the RAS-MAPK or PI3K-Akt pathway and results in the induction of Snail [27,28].”
Derailed endocytosis: an emerging feature of cancer (2008, background): “An illustrative example relates to EGF-stimulated epidermoid cells: following stimulation, SNAIL is slowly induced and represses E-cadherin expression, but existing junctional E-cadherin rapidly undergoes endocytosi”
PKM2 Phosphorylates Histone H3 and Promotes Gene Transcription and Tumorigenesis (2012, positive): “EGFR activation results in GSK-3b-independent b-catenin transactivation by mechanisms that are distinct from Wntdependent canonical signaling (Fang et al., 2007; Ji et al., 2009; Lu et al., 2003; Lu and Hunter, 2004; Yang et al., 2011).”
Signaling mechanisms of the epithelial-mesenchymal transition (2014, background): “Upon binding of EGF to its receptor, E-cadherin is internalized from the cell membrane, reducing cell-cell contacts and weakening the epithelial layer (152).”
Epidermal growth factor receptor cooperates with signal transducer and activator of transcription 3 to induce epithelial-mesenchymal transition in cancer cells via up-regulation of TWIST gene expression. (2007, neutral): “in A431 human epidermoid carcinoma cells (10).”
New signals from the invasive front (2006, background): “Some of these repressors are specifically expressed at the invasive front of human cancers, and their expression seems to be highly regulated by pathways known to promote tumour progression, including Wnt, TGF-β, FGF, EGF, signal transducer and activator of transcription 3 (STAT3) and nuclear factor”