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AKT1 — 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
Grille et al., J Soc Biol 2004
:
[
Regulation of
E-cadherin by the Akt
protein kinase B ]
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 ... 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