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EGF — FOS

Text-mined interactions from Literome

Hsieh et al., Int J Cancer 2000 (Ovarian Neoplasms) : The duration of EGF mediated c-Fos mRNA up-regulation was decreased in parallel with loss of ErbB-2 expression
Gründker et al., Gynecol Oncol 2000 (Genital Neoplasms, Female) : In all of the lines expressing LHRH receptor, EGF induced c-fos mRNA expression as well as c-Fos protein synthesis was dose-dependently reduced by treatment with LHRH agonists and antagonists
Bode et al., Cancer Res 2001 (Cell Transformation, Neoplastic) : The purpose of this study was to investigate the effect of two structurally related compounds of the ginger family, [ 6 ] -gingerol and [ 6 ] -paradol, on EGF induced cell transformation and AP-1 activation
Aigner et al., Oncogene 2001 (Breast Neoplasms...) : In parallel, EGF induced activation of p44/p42 MAP-kinases and activation of c-Fos expression were increased in ribozyme transfected MKN7 cells
Liu et al., Proc Natl Acad Sci U S A 2001 (Cell Transformation, Neoplastic) : AA treatment had no effect on either TPA- or EGF induced AP-1 transactivation or transformation, but did abrogate the inhibitory effects of DHA on TPA- or EGF induced AP-1 transactivation and cell transformation in a dose dependent manner
Liu et al., Cancer Res 2001 (Cell Transformation, Neoplastic...) : Two novel glycosides, 6-O- ( beta-D-glucopyranosyl ) -1-O-octanoyl-beta-D-glucopyranose and asperulosidic acid, extracted from the juice of noni fruits, were used to examine their effects on 12-O-tedtradecanoylphorbol-13-acetate ( TPA ) - and epidermal growth factor (EGF) induced AP-1 transactivation and cell transformation in mouse epidermal JB6 cells ... TPA- or EGF induced phosphorylation of c-Jun, but not extracellular signal regulated kinases or p38 kinases, was also blocked by the compounds, indicating that c-Jun N-terminal kinases were critical in mediating TPA- or EGF induced AP-1 activity and subsequent cell transformation in JB6 cells
Bancroft et al., Int J Cancer 2002 (Carcinoma, Squamous Cell...) : In our study, we examined the effect of EGF and antagonists of EGFR, PI3K and MEK on NF-kappaB and AP-1 activation and IL-8 and VEGF expression in HNSCC cell lines UM-SCC-9 and 11B in which EGFR is overexpressed and activated ... 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
Dhar et al., Mol Cell Biochem 2002 (Cell Transformation, Neoplastic...) : TPA and EGF , acting through the MAP kinase pathway, activate AP-1 and subsequently NF-kappaB proteins and downstream transcription processes that are involved in the transformation response in transformation-sensitive ( P+ ) JB6 cells
Shiratsuchi et al., J Cell Physiol 2002 (Carcinoma, Squamous Cell...) : EGF also induced increased expression of uPA and uPA receptor (uPAR) proteins and mRNA, as well as transcription factor activator protein-1 (AP-1)-DNA binding
Pandey et al., Oncogene 2002 : Overexpression of Odin, but not an unrelated adapter protein, Grb2, inhibited EGF induced activation of c-Fos promoter
Kim et al., J Biol Chem 2003 : In addition, ARF4 mediated PLD2 activation leads to dramatic activation of the transcription factor activator protein 1 (AP-1), and, importantly, ARF4 activity is required for EGF induced activation of cellular AP-1
Li et al., Oncogene 2003 : We demonstrated that the TPA or epidermal growth factor (EGF) induced AP-1 activation in the B82L cells that express wild-type EGFR, but not in the B82 cell, whereas autophosphorylation at tyrosine ( 1173 ) of EGFR in B82L cells was only induced by EGF, but not TPA ... The expression of tyrosine kinase-deficient EGFR ( mutation at Lys-721 ) ( B82M721 ) resulted in deficiency of AP-1 induction in cellular response to EGF , while TPA treatment led to fully 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
Ediger et al., Eur Respir J 2003 (Cell Transformation, Neoplastic...) : LPA and EGF both activated activator protein (AP)-1 , cyclic adenosine monophosphate response element binding protein, nuclear factor of activated T-cells and the serum response element ; however, only AP-1 activation exhibited synergism
Ben-Ari et al., Mol Carcinog 1992 (Cell Transformation, Neoplastic) : The activity of AP-1 , a trans acting transcription factor, is stimulated by 12-O-tetradecanoylphorbol-13-acetate ( TPA ) and epidermal growth factor (EGF) in promotion-sensitive ( P+ ) but not in promotion-resistant ( P- ) JB6 mouse epidermal cell lines
Ma et al., Biochem Pharmacol 2005 : EGF activated AP-1 only in B82L cells ; the activation was mediated primarily by Akt and ERK ... Ethanol inhibited EGF induced EGFR autophosphorylation, phosphorylation of ERK as well as Akt and its substrate GSK-3beta, and subsequently blocked EGF stimulated AP-1 activation in B82L cells
Zhao et al., J Biol Chem 2005 (Cell Transformation, Neoplastic) : Interestingly, 2-AG enhanced epidermal growth factor induced AP-1 DNA binding and cell transformation
Shi et al., Exp Dermatol 2005 (MAP Kinase Signaling System) : Epidermal growth factor (EGF) mediated DNA binding activity of AP-1 is attenuated in senescent human epidermal keratinocytes
Singh et al., Mol Cancer Ther 2006 (MAP Kinase Signaling System) : Silibinin treatment under similar conditions also strongly inhibited EGF induced ERK1/2, JNK1/2, and p38K as well as Akt phosphorylation, and also suppressed EGF induced AP-1 and NF-kappaB activation
Takeuchi et al., FEBS J 2006 (Adenocarcinoma...) : Expression of the c-Fos and c-Jun, components of activator protein 1 (AP1), which are known to regulate bcl-X ( L ) gene transcription, were increased in response to EGF ... Pretreatment of the cells with PD98059, an inhibitor of MAP kinase kinase, inhibited the EGF induced c-Fos and c-Jun expression, AP1 DNA binding, Bcl-X ( L ) expression, and the resistance against ADR induced apoptosis, suggesting that EGF transmitted the antiapoptotic signal in such a way that it activated AP1 via a MAP kinase signaling pathway
Hornberg et al., Mol Biotechnol 2006 : EGF could not induce AP-1 activity or S-phase entry in density arrested cells, but could do so after pretreatment with retinoic acid, which enhances EGF receptor expression ... Our results support a model in which the EGF receptor regulates density dependent growth control in NRK fibroblasts, which is reflected by EGF induced mitogenic signaling and consequent AP-1 activity
den Hertog et al., Nucleic Acids Res 1992 : Here we demonstrate that Jun B is the only member of the Jun- and Fos-families that is induced by Epidermal Growth Factor (EGF) in transfected murine P19 EC cells, expressing functional human EGF receptors ( hEGF-Rs )
Nomura et al., Anticancer Res 2007 (Cell Transformation, Neoplastic) : Tetrandrine significantly blocked EGF induced cell transformation, attenuated EGF induced AP-1 activation, and inhibited phosphorylation of ERKs, which regulates AP-1 activation
Chen et al., Am J Physiol Endocrinol Metab 2009 : Furthermore, E2 did not affect the ability of EGF to induce c-Fos expression or modulate AP-1 activity
van Houdt et al., Neoplasia (New York, N.Y.) 2010 (Colorectal Neoplasms) : Deletion of oncogenic KRAS not only resensitized tumor cells to EGFR inhibition but also promoted EGF induced NRAS activation, ERK and AKT phosphorylation, and c-FOS transcription
Ikari et al., Biochim Biophys Acta 2011 : U0126, a MEK inhibitor, inhibited EGF induced increases in c-Fos , p-ERK, and TRPM6 levels ... In contrast, neither rapamycin nor LY-294002 inhibited EGF induced increases in p-ERK and c-Fos levels
Mahadevan et al., Oncogene 1990 : Further, we show here that although EGF- and TPA stimulated induction of c-fos is abolished by 2-aminopurine, the appearance of TRE binding activity in nuclear extracts of stimulated cells is unaffected, suggesting that EGF- and TPA stimulated induction of TRE binding activity utilises existing proteins and is not dependent on fresh c-FOS synthesis
Kang et al., Clin Cancer Res 2011 (Neoplasms, Experimental...) : We confirmed a constitutive activation of RAF/MEK/ERK ( extracellular signal regulated kinase ) in YAP1 expressing MKN45 cells and further showed that YAP1 enhanced serum/epidermal growth factor induced c-Fos expression in gastric cancer cells
Haim et al., Neoplasia (New York, N.Y.) 2011 (Breast Neoplasms) : In parallel, in the joint stimulation, EGF acted independently at the transcription level through AP-1 , to upregulate CXCL8 expression
Khanal et al., Mol Carcinog 2011 (Cell Transformation, Neoplastic...) : In addition, 5'-NIO exerted strong inhibitory effects on the EGF- or TPA induced c-fos or c-jun transcriptional activity, and thereby inhibited the associated activator protein-1 (AP-1) transactivation activity induced by EGF or TPA
Hwang et al., Mol Nutr Food Res 2011 (Fibrosarcoma...) : Capsaicin suppressed EGF induced c-Jun and c-Fos nuclear translocation, and also abrogated the EGF induced phosphorylation of EGF receptor (EGFR), focal adhesion kinase ( FAK ), protein kinase C ( PKC ), phosphatidylinositol 3-Kinase (PI3K)/Akt, extracellular regulated kinase (ERK)1/2, and JNK1/2, an upstream modulator of AP-1 ... Furthermore, the EGFR inhibitor inhibited EGF induced MMP-9 expression, as well as AP-1 activity and cell migration
Yoshida et al., Jpn J Cancer Res 1990 (Carcinoma...) : Both EGF and TGF-alpha stimulated EGFR phosphorylation, EGF and TGF-alpha induced FOS , MYC and ERBB-2 oncogene expression
Mullenbrock et al., J Biol Chem 2011 (MAP Kinase Signaling System) : Expression of several AP-1 family members was induced by both EGF and NGF, but their induction was more robust and sustained in response to NGF
Tarcic et al., FASEB J 2012 : In addition to strong activation of ERK by EGF, and AKT by serum, early transcription remarkably differed : while EGF induced early growth response-1 (EGR1), and this was required for migration, serum induced c-Fos and FosB to enhance proliferation
Peng et al., J Biol Chem 2012 (Cell Transformation, Neoplastic...) : Knockdown of TRAF2 blocked EGF induced AP-1 activity and anchorage- independent cell transformation
Saxena et al., Antioxid Redox Signal 2013 (Colonic Neoplasms...) : Inhibition of AR also prevented the epidermal growth factor induced phosphorylation of phosphatidylinositol 3-kinase (PI3K), serine/threonine kinase ( AKT ), c-Jun, c-Fos , PTEN, and FOXO3a, and deoxyribonucleic acid ( DNA ) -binding activity of AP-1
Baptist et al., Exp Cell Res 1995 : ( i ) EGF and HGF induced c-Fos accumulation and MAP kinase translocation in variable fractions of the cell population that corresponded to their relative potency as mitogens ... This reflected the fact that EGF induced c-Fos accumulation in 90 % of cells in the presence of forskolin but in 30-50 % of cells in its absence
Peto et al., J Gen Virol 1995 (Disease Progression...) : Mutating either AP-1 site in the complete enhancer decreases the EGF response, whereas a double mutation causes a complete loss of EGF regulation, suggesting that the EGF induction of HPV-16 early transcription requires AP-1 activation
Yamada et al., Eur J Neurosci 1995 : Among the cultured cortical neurons, we observed neurons possessing the EGF receptor and cells expressing c-Fos protein in response to EGF
Huang et al., Mol Cell Biol 1996 (Cell Transformation, Neoplastic) : Requirement for phosphatidylinositol 3-kinase in epidermal growth factor induced AP-1 transactivation and transformation in JB6 P+ cells ... ( i ) EGF not only induced a high level of PI 3-kinase activity by itself but also enhanced insulin induced PI 3-kinase activity in JB6 P+ cells, the EGF induced PI-3 kinase activity could be blocked by constitutive overexpression of a dominant negative P85 subunit of PI 3-kinase ( deltaP85 ), and insulin could markedly promote EGF induced AP-1 activity in a dose dependent manner in JB6 P+ cells as well as promote EGF induced JB6 P+ cell transformation ... ( ii ) Inhibition of PI-3 kinase with wortmannin or LY294002 markedly decreased the AP-1 activity induced by insulin, EGF , or EGF and insulin in a dose dependent manner, while wortmannin did not block UVB induced AP-1 activity ... ( iii ) AP-1 activation by insulin, EGF , or EGF and insulin could be completely inhibited by overexpression of deltaP85 in all the dose and time courses studied ... These results demonstrate for the first time that PI 3-kinase appears to be required for EGF- or insulin induced AP-1 transactivation and cell transformation but not cell proliferation in JB6 cells
Huang et al., J Biol Chem 1996 : Since UVB is responsible for most of the carcinogenic effects of sun exposure, we investigated the role of EGF receptors and PKC in UVB induced AP-1 activation ... All of this evidence indicated that aPKC, but not EGF receptor, is involved in UVB induced AP-1 activation
Marks et al., Am J Physiol 1996 : Fos is required for EGF stimulation of the gastrin promoter ... We found that epidermal growth factor (EGF) and tumor necrosis factor-alpha (TNF-alpha) transiently stimulate an increase in Fos protein that precedes stimulation of the gastrin promoter
Elliget et al., Cell Growth Differ 1996 (Carcinoma, Squamous Cell) : A431 human epidermoid carcinoma cells were treated with TGF beta and epidermal growth factor (EGF) ( 10 ng/ml each ) to determine if TGF beta modulates EGF induced Ca2+ signaling and c-Fos oncoprotein levels
Huang et al., Oncogene 1997 : Signal transduction through atypical PKCs, but not the EGF receptor, is necessary for UVC induced AP-1 activation in immortal murine cells ... This was found at all UVC irradiation doses and time courses studied, while high levels of EGF induced AP-1 activity were observed in B82L cells but not in B82 cells ... This evidence strongly suggests that atypical PKCs, but not the EGF receptor, is necessary for UVC induced AP-1 activation in JB6 and B82 cells
Agadir et al., Cancer Res 1997 (Breast Neoplasms) : Furthermore, using gel retardation assay, we show that 12-O-tetradecanoylphorbol-13-acetate- and epidermal growth factor induced AP-1 binding activity in breast cancer cells is inhibited by RME
Major et al., J Pharmacol Exp Ther 1997 : However, EGF stimulated receptor autophosphorylation of mitogen activated protein kinase phosphorylation and c-Fos protein expression were not inhibited by CGP 53716 at 1 or 10 microM in RASMC
Huang et al., Proc Natl Acad Sci U S A 1997 : The inhibition appears to be specific for UV-induced signal transduction for AP-1 activation, because these inhibitors did not block UV-induced p53 activation nor did they exhibit any significant influence on epidermal growth factor induced AP-1 transactivation
Nadori et al., Hepatology 1997 : We therefore compared in primary and transformed rat hepatocytes ( 1 ) the composition of AP-1 dimers under basal conditions and ( 2 ) AP-1 induction by epidermal growth factor (EGF) ... In both cell types, activation of AP-1 DNA binding activity by EGF was accompanied by the recruitment of Fra-1 into AP-1, detected earlier in 7777 cells than in hepatocytes, and with the transient appearance of c-Fos in 7777 cells only
Hong et al., Toxicology 1998 : The combination of ciprofibrate and PGF2alpha blocked the inhibitory effect of transforming growth factor ( TGF ) -beta on the DNA binding activity of AP-1 induced by EGF