Gene interactions and pathways from curated databases and text-mining

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CDH1 — STAT3

Text-mined interactions from Literome

Sultan et al., Oncogene 2005 (Breast Neoplasms...) : Inducible E-cadherin was blocked by dominant negative ( Dn ) Stat5 or Dn-Jak2, but not by Dn-Stat3
Arulanandam et al., Mol Cancer Res 2009 : In the present report, we show that Stat3 can also be activated through homophilic interactions by the epithelial (E)-cadherin ... Indeed, by plating cells onto surfaces coated with fragments encompassing the two outermost domains of this cadherin, we clearly show that cadherin engagement can activate Stat3 , even in the absence of direct cell-to-cell contact
Xiong et al., J Biol Chem 2012 (Colorectal Neoplasms...) : Roles of STAT3 and ZEB1 proteins in E-cadherin down-regulation and human colorectal cancer epithelial-mesenchymal transition ... In this study, we examined the roles of STAT3 in CRC EMT and ZEB1, an EMT inducer, in STAT3 induced down-regulation of E-cadherin ... Meanwhile, overexpression of STAT3 significantly reduced E-cadherin and enhanced N-cadherin and vimentin expressions in weakly invasive SW1116 CRC cells ... STAT3 regulated ZEB1 expression in CRC cells, and the STAT3 induced decrease in E-cadherin and cell invasion depended on activation of ZEB1 in CRC cells ... ZEB1 may participate in STAT3 induced cell invasion and E-cadherin down-regulation in CRC cells
Geletu et al., Biochim Biophys Acta 2013 (MAP Kinase Signaling System) : We recently demonstrated that engagement of E-cadherin , a calcium dependent, cell to cell adhesion molecule which is often required for cells to remain tightly associated within the epithelium, also activates Stat3 ... We recently demonstrated that engagement of E-cadherin , a calcium dependent, cell to cell adhesion molecule which is often required for cells to remain tightly associated within the epithelium, also activates Stat3