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CDH1 — PIK3R1
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
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
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 ... 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
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