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AKT3 — CDH1

Text-mined interactions from Literome

Reddy et al., Mol Endocrinol 2005 (MAP Kinase Signaling System...) : Akt activation is mediated through the activation of phosphatidylinositol 3 kinase, and both Akt and MAPK activation are mediated by an E-cadherin adhesion induced ligand independent activation of epidermal growth factor receptor
Strizzi et al., J Cell Sci 2005 (Mammary Neoplasms, Animal) : Treating EpH4/Cripto-1 or HC-11/Cripto-1 mammary cells with exogenous soluble Netrin-1 resulted in increased expression of E-cadherin and UNC5H1, decreased expression of vimentin and decreased activation of Akt as determined by western blotting
Imanishi et al., Cancer Res 2007 (Breast Neoplasms...) : Using a xenograft model, we show that overexpression of Ang2 in poorly metastatic MCF-7 breast cancer cells suppresses expression of E-cadherin and induces Snail expression and phosphorylation of Akt and glycogen synthase kinase-3beta ( GSK-3beta ) promoting metastasis to the lymph nodes and lung
Chae et al., Biochem Biophys Res Commun 2009 : With increasing expression of adherens junction components of E-cadherin and beta-catenin, E-cadherin and p-Akt expression increased in 7 days post-confluent Caco-2 cells, and in human intestinal tissue, expression of E-cadherin and p-Akt also increased in the upper portion of villi, compared to the crypt
De Santis et al., Oncogene 2009 (Ovarian Neoplasms) : E-cadherin directly contributes to PI3K/AKT activation by engaging the PI3K-p85 regulatory subunit to adherens junctions of ovarian carcinoma cells
Hong et al., J Exp Clin Cancer Res 2009 (Carcinoma, Squamous Cell...) : This study aimed to investigate whether Akt inhibition would restore the expression of E-cadherin and beta-catenin, reduce that of Vimentin, and induce the MErT in OSCC cells with low or negative expression of E-cadherin
Zhou et al., Mol Cancer Ther 2009 (Lung Neoplasms...) : Luteolin inhibits mdm2 through AKT and overexpression of active AKT attenuated luteolin induced expression of E-cadherin , suggesting that luteolin regulates E-cadherin through AKT/mdm2 pathway ... Luteolin inhibits mdm2 through AKT and overexpression of active AKT attenuated luteolin induced expression of E-cadherin , suggesting that luteolin regulates E-cadherin through AKT/mdm2 pathway
Georgopoulos et al., PloS one 2010 : Functional inactivation of E-cadherin interferes with the capacity of NHU cells to form stable calcium mediated contacts, attenuates E-cadherin mediated PI3-K/AKT induction and enhances NHU cell proliferation by allowing de-repression of the EGFR/ERK pathway and constitutive activation of ß-catenin-TCF signalling
Lau et al., Oncogene 2011 (Ovarian Neoplasms) : E-cadherin inhibits tumor cell growth by suppressing PI3K/Akt signaling via ß-catenin-Egr1 mediated PTEN expression ... In this study, we showed that loss of E-cadherin induced ovarian cancer cell growth and constitutive activation of phosphoinositide 3-kinase (PI3K)/Akt signaling by the inhibition of phosphatase and tensin homolog (PTEN) transcription through the downregulation of early growth response gene 1 (Egr1) ... Thus, the loss of E-cadherin itself may contribute to dysregulated PI3K/Akt signaling through its effects on PTEN, or it may exacerbate the frequent activation of PI3K/Akt signaling that occurs as a result of overexpression, mutation and/or amplification
Xing et al., Oncogene 2011 (Breast Neoplasms...) : Notably, a ?-secretase inhibitor significantly blocked Notch mediated invasion and survival under hypoxia by promoting expression of E-cadherin and inhibiting Akt phosphorylation
Cheng et al., J Clin Endocrinol Metab 2012 : Moreover, the inhibition of EGF induced ERK1/2, p38, and Akt activation by pharmacological inhibitors attenuated EGF induced Slug expression and the down-regulation of E-cadherin , as well as subsequent cell invasion ... Moreover, the inhibition of EGF induced ERK1/2, p38, and Akt activation by pharmacological inhibitors attenuated EGF induced Slug expression and the down-regulation of E-cadherin , as well as subsequent cell invasion
Kisslov et al., Biochim Biophys Acta 2012 (Colonic Neoplasms) : AS or Ly294002, but not H-89, decreased PKB/Akt activation as well as the nuclear localization of ß-catenin and cyclin D1 and increased the plasma membrane localization of ß-catenin with E-cadherin , suggesting that these processes are regulated by the PKB pathway
Chen et al., Mol Med Report 2013 (Breast Neoplasms) : miRNA-200c increases the sensitivity of breast cancer cells to doxorubicin through the suppression of E-cadherin mediated PTEN/Akt signaling
Lau et al., PloS one 2013 (Neoplasm Invasiveness...) : The pharmacological inhibition of phosphatidylinositol-3-kinase (PI3K), mammalian target of rapamycin (mTOR), and MEK suggests that both PI3K/Akt/mTOR and MAPK/ERK signaling are required for FGF2 induced E-cadherin down-regulation
Yan et al., PloS one 2013 : Additionally, inhibition of AKT activation significantly enhanced E-cadherin expression, an observation that mimics the situation observed in contactin-1 knockdown, suggesting that activation of AKT plays a role in contactin-1 mediated downregulation of E-cadherin