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FOS — SPP1
Text-mined interactions from Literome
Kim et al., J Cell Biochem 2002
:
Okadaic acid stimulates
osteopontin expression through de novo
induction of
AP-1
Renault et al., Circ Res 2003
:
AP-1 is
involved in UTP induced
osteopontin expression in arterial smooth muscle cells
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 ...
OPN induced ERK phosphorylation,
AP-1 activation, uPA secretion, and cell motility were suppressed when cells were transfected with dn c-Src or pretreated with alpha(v)beta(3) integrin antibody, c-Src kinase inhibitor ( pp2 ), EGFR tyrosine kinase inhibitor ( PD153035 ), and MEK-1 inhibitor ( PD98059 ) ... To our knowledge, this is the first report that
OPN induces alpha(v)beta(3) integrin mediated
AP-1 activity and uPA secretion by activating c-Src/EGFR/ERK signaling pathways and further demonstrates a functional molecular link between OPN induced integrin/c-Src dependent EGFR phosphorylation and ERK/AP-1 mediated uPA secretion, and all of these ultimately control the motility of breast cancer cells
Rangaswami et al., J Biol Chem 2005
(Neoplasm Invasiveness) :
To our knowledge this is first report that
OPN induces NIK/MEKK1 mediated JNK1 dependent/independent
AP-1 mediated pro-MMP-9 activation and regulates the negative crosstalk between NIK/ERK1/2 and MEKK1/JNK1 pathways that ultimately controls the cell motility, invasiveness, and tumor growth
Takeshita et al., J Oral Sci 2005
(Second Messenger Systems) :
Sphingosine 1-phosphate ( SPP ) actually induced expression of these oncogenes and
activated AP-1
Hartl et al., Oncogene 2006
(Cell Transformation, Neoplastic...) :
Electrophoretic mobility shift assays, chromatin immunoprecipitation and transcriptional reporter gene analyses showed that
c-Fos and c-Jun bind specifically to this site and that c-Fos efficiently
transactivates the
OPN promoter
Jalvy et al., Circ Res 2007
(MAP Kinase Signaling System) :
We previously demonstrated that
osteopontin (OPN) expression is a key step for UTP mediated migration of arterial SMCs and that
activator protein (AP)-1 , nuclear factor kappaB, and upstream stimulatory transcription factors are
involved in this OPN expression
Rangaswami et al., Oncol Rep 2007
(Lung Neoplasms...) :
OPN triggers NIK- and MEKK1 dependent
AP-1 activation whereas NIK dependent AP-1 activation is independent of JNK1 that leads to pro-MMP-9 activation
Ahmed et al., Molecular cancer 2010
(Breast Neoplasms) :
Moreover, overexpression of mTOR inhibits
OPN induced NF-kappaB and
AP-1-DNA binding and transcriptional activity
Sharma et al., Molecular cancer 2010
:
Silencing HDAC1 followed by stimulation with PMA resulted in significant decrease in OPN promoter activity suggesting that HDAC1 but not HDAC3 or HDAC4 was required for
AP-1 mediated
OPN transcription
Tachibana et al., J Am Soc Nephrol 2012
(Diabetes Mellitus, Experimental...) :
In vitro, LXR activation suppressed osteopontin expression in proximal tubular epithelial cells by inhibiting
AP-1 dependent transcriptional activation of the
osteopontin promoter