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EGFR — JUN
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Murasawa et al., J Biol Chem 2000
(Calcium Signaling) :
In this study, we tested the
involvement of Pyk2 and
EGF-R in Ang II-induced activation of JNK and
c-Jun in cardiac fibroblasts
Chen et al., J Biol Chem 2001
:
c-Jun N-terminal kinase activation by hydrogen peroxide in endothelial cells
involves SRC dependent
epidermal growth factor receptor transactivation
Chen et al., J Biol Chem 2001
(Cell Transformation, Neoplastic) :
Egfr gene deficiency
blocked TPA induced ERK activity and
AP-1 binding activity
Bancroft et al., Int J Cancer 2002
(Carcinoma, Squamous Cell...) :
Recombinant EGF induced
EGFR phosphorylation,
activation of NF-kappaB and
AP-1 reporter genes and IL-8 and VEGF expression, indicating that EGFR can mediate coactivation of both transcription factors and cytokine genes in HNSCC ... We conclude that antagonists of EGFR, PI3K and MEK signal pathways have inhibitory activity against
EGFR induced NF-kappaB and
AP-1 activation, IL-8 and VEGF expression and growth by HNSCC
Li et al., Oncogene 2003
:
Currently, little is known about whether
EGFR or its tyrosine kinase is
necessary for TPA induced
AP-1 activation ... Based on these results, we conclude that TPA induced AP-1 activation requires the basal level-EGFR protein, but not EGFR tyrosine kinase and EGFR autophosphorylation at tyrosine ( 1173 ), whereas both EGFR tyrosine kinase and
EGFR autophosphorylation at Y ( 1173 )
play a critical role in EGF induced
AP-1 activation
Zenz et al., Dev Cell 2003
(Genetic Predisposition to Disease...) :
Thus, using three experimental systems, we show that
EGFR and HB-EGF are
regulated by
c-Jun , which controls eyelid development, keratinocyte proliferation, and skin tumor formation
Das et al., J Biol Chem 2004
(Breast Neoplasms...) :
Furthermore, OPN induces alpha(v)beta(3)
integrin/EGFR mediated ERK1/2 phosphorylation and
AP-1 activation
Cuadrado et al., Oncogene 2004
(Breast Neoplasms) :
In contrast, induction of
c-JUN does not
require EGFR activity and p65/RELA induction is only partially dependent on these kinases
Ma et al., Biochem Pharmacol 2005
:
The
role of
epidermal growth factor receptor in ethanol mediated inhibition of
activator protein-1 transactivation ... Thus,
EGFR plays a critical role in the interaction between ethanol and
AP-1
Song et al., Oncogene 2005
:
We found that BPDE induced COX-2 expression was through inhibition of RAR-beta ( 2 ) and consequently,
induction of
epidermal growth factor receptor (EGFR) , extracellular signal regulated protein kinases 1/2 ( Erk1/2 ) phosphorylation, and
c-Jun expression
Reinehr et al., Gastroenterology 2005
:
Consequences of TLCS induced oxidative stress were
c-Jun-N-terminal kinase activation and Yes dependent
activation of the
epidermal growth factor receptor (EGFR) , followed by EGFR catalyzed CD95 tyrosine phosphorylation, formation of the death inducing signaling complex, and execution of apoptosis
Finch et al., Free Radic Biol Med 2006
(Carcinoma, Squamous Cell) :
An
EGF-R inhibitor, AG1478,
blocks the higher
AP-1 transactivation and cell proliferation of the low catalase 6M90 cells
Jiang et al., J Ocul Pharmacol Ther 2006
:
EGF induced cell migration in a dose dependent manner ; EGF induced
EGFR phosphorylation and downstream
activation of
c-Jun N-terminal protein kinase (JNK) , p38 MAP kinase ( p38 ), extracellular signal regulated kinase ( ERK1/2 ) and AKT, were inhibited by PD153035 ( EGFR inhibitor ), JNKi ( JNK inhibitor ), SB203580 ( p38 inhibitor ), U0126 ( MEK/ERK inhibitor ), and LY294002 ( PI3K/AKT inhibitor ), respectively
Ogunwobi et al., Endocrinology 2006
(Adenocarcinoma...) :
Leptin stimulates proliferation and inhibits apoptosis in Barrett 's esophageal adenocarcinoma cells by cyclooxygenase-2 dependent, prostaglandin-E2 mediated transactivation of the
epidermal growth factor receptor and
c-Jun NH2-terminal kinase
activation
Hornberg et al., Mol Biotechnol 2006
:
Epidermal growth factor receptor induced
activator protein 1 activity controls density dependent growth inhibition in normal rat kidney fibroblasts
Joo et al., Oncogene 2008
:
Finally,
EGFR transactivation was
involved in the expression of c-Fos and
c-Jun via the extracellular signal regulated kinase signaling cascade
Reinehr et al., Methods Enzymol 2007
:
Hyperosmolarity induced ROS formation then leads to a Src-family kinase Yes mediated activation of the
epidermal growth factor receptor (EGFR) and to an
activation of the
c-Jun-N-terminal kinase (JNK)
Hsieh et al., J Cell Biochem 2008
:
Moreover, S1P induced
EGFR expression was
inhibited by an
AP-1 inhibitor curcumin and tanshinone IIA
Hsieh et al., Biochim Biophys Acta 2008
:
Moreover, thrombin stimulated
activation of NF-kappaB,
AP-1 , and COX-2 promoter activity was blocked by the inhibitors of c-Src, PKC,
EGFR , MEK1/2, AP-1 and NF-kappaB, suggesting that thrombin induces COX-2 promoter activity mediated through PKC ( delta ) /c-Src dependent EGFR transactivation, MEK-ERK1/2, AP-1, and NF-kappaB
Schnidar et al., Cancer Res 2009
(Cell Transformation, Neoplastic...) :
EGFR/MEK/ERK signaling
induces JUN/activator protein 1 activation, which is essential for oncogenic transformation, in combination with the GLI activator forms GLI1 and GLI2
Kajanne et al., Int J Oncol 2009
(Prostatic Neoplasms) :
Here, we show that constitutive
AP-1 activity in prostate cancer cells is
dependent on the activities of
EGF-R and PI3K ... Together, the findings show that
AP-1 activity in prostate cancer cells
mediates EGF-R and PI3K signalling, is essential for their proliferation, and confers protection against radiation induced cell death
Mascia et al., J Invest Dermatol 2010
(Dermatitis, Atopic...) :
Furthermore,
EGFR activation
enhanced TNF-alpha induced
c-Jun phosphorylation and DNA binding, whereas c-Jun silencing reduced GM-CSF expression
Oyesanya et al., Molecular cancer 2010
(Neoplasm Invasiveness) :
In ovarian cancer cells highly responsive to LPA, activation of
AP-1 by LPA was
suppressed by inhibition of
EGFR , an effect that could be reversed by co-stimulation of another receptor tyrosine kinase c-Met with hepatocyte growth factor, indicating that LPA mediated activation of AP-1 requires activity of a RTK, not necessarily EGFR
Naderi et al., Int J Cancer 2012
(Breast Neoplasms) :
In this feedback loop,
ErbB2 overexpression
results in an induction of
c-Jun and BEX2 expression
Hwang et al., Mol Nutr Food Res 2011
(Fibrosarcoma...) :
Furthermore, the
EGFR inhibitor
inhibited EGF induced MMP-9 expression, as well as
AP-1 activity and cell migration ... Capsaicin inhibited the EGF induced invasion and migration of human fibrosarcoma cells via
EGFR dependent FAK/Akt, PKC/Raf/ERK, p38 mitogen activated protein kinase ( MAPK ), and
AP-1 signaling, leading to the down-regulation of MMP-9 expression
Saeki et al., Exp Dermatol 2012
:
In the current study, the regulatory relationship between
ErbB receptor activation and
induction of
AP-1 proteins in calcium dependent keratinocyte differentiation was analysed ... The predicted network showed that the
ErbB receptor might
regulate AP-1 protein expression via two pathways : positive regulation by c-MYC and negative regulation by signal transducer and activator of transcription 3 ( STAT3 ) pathways ... Experimental validation analysis revealed that
ErbB receptor inhibition
resulted in defective induction of
AP-1 proteins and suppressed terminal differentiation of keratinocytes
Okimoto et al., Oncogene 1996
:
Regulation of
epidermal growth factor receptor by activated H-ras and V-myc oncogenes in mouse Balb/3T3 cells : possible
roles of
AP-1