◀ Back to EGFR
EGFR — PTEN
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
McKenna et al., Semin Oncol 2003
(Colorectal Neoplasms) :
In addition to
EGFR and Ras,
PTEN can also
regulate the PI3K pathway
McKenna et al., Oncogene 2003
(Neoplasms) :
In addition to
EGFR and RAS,
PTEN can also
regulate the PI3K pathway
McKenna et al., Genes Chromosomes Cancer 2003
(Neoplasms) :
In addition to
EGFR and RAS,
PTEN can also
regulate the PI3 kinase pathway
Fiano et al., Anticancer Res 2004
(Central Nervous System Neoplasms...) :
PTEN lipid phosphatase degrades PIP3 and negatively regulates Akt, whereas this is
activated by
EGFR through PI3
Dackour et al., In Vitro Cell Dev Biol Anim 2005
(Laryngeal Neoplasms...) :
Papilloma cells overexpress the
EGFR and have constitutively active extracellular signal regulated kinase ( ERK ) and enhanced phosphatidylinositol 3-kinase (PI3K) activity, but overexpression of the lipid phosphatase
PTEN ( Phosphatase and Tensin Homolog )
reduces activation of Akt by PI3K
Li et al., Zhonghua Zhong Liu Za Zhi 2006
(Pancreatic Neoplasms) :
Exogenous
PTEN can block ASPC-1 cell cycle at the G(2)/M phase, enhance the cell apoptosis induced by hypoxia,
inhibit the expression of VEGF and
EGFR proteins under hypoxic condition, and inhibit the proliferation and growth of ASPC-1 cells
Sos et al., Cancer Res 2009
(Carcinoma, Non-Small-Cell Lung...) :
We show that in EGFR dependent cells,
PTEN loss partially uncouples mutant EGFR from downstream signaling and
activates EGFR , thereby contributing to erlotinib resistance
Han et al., J Biol Chem 2010
(Skin Neoplasms) :
CsA induced
PTEN down-regulation occurs at the transcription level and is
epidermal growth factor receptor dependent
Vivanco et al., Proc Natl Acad Sci U S A 2010
:
The
phosphatase and tensin homolog regulates
epidermal growth factor receptor (EGFR) inhibitor response by targeting EGFR for degradation
Feng et al., Cancer Sci 2010
(Colonic Neoplasms) :
The levels of both phosphorylated and total
EGFR were
increased when HCT116 cells ectopically overexpressed Spry2, with concomitant increase in
phosphatase and tensin homolog (PTEN) expression
Li et al., Mol Cell Biochem 2012
(Endometrial Neoplasms) :
Loss of
PTEN promoted cell proliferation and
led to significant increases in the levels of
EGFR , phospho-EGFR, AKT, phospho-AKT, and phospho-mTOR proteins
Cathomas et al., Clin Cancer Res 2012
(Neoplasm Metastasis...) :
A potential correlation between EGFR overexpression, persistent expression of
PTEN , and
EGFR inhibition should be investigated further