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CCND1 — JUN
Pathways - manually collected, often from reviews:
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Lee et al., J Biol Chem 1999
(Breast Neoplasms) :
Dominant negative mutants of CREB and ATF-2 but not
c-Jun inhibited pp60 ( v-src ) induction of
cyclin D1
Balmanno et al., Oncogene 1999
:
This suggests that both early and late
AP-1 gene expression is regulated by the same Gi-mediated, MEK dependent MAPK signalling pathway but that expression of late AP-1 genes and
cyclin D1 requires that this pathway be persistently activated
Sabbah et al., Proc Natl Acad Sci U S A 1999
:
Both
c-Jun and ATF-2
transactivated the
cyclin D1 promoter in transient transfection experiments, and a clear additional increase was detected when ER was cotransfected with either c-Jun or with c-Jun and ATF-2 but not with ATF-2 alone ... To interpret these results, we propose a mechanism in which
ATF-2/c-Jun heterodimers bind to the CRE-D1 element and
mediate the activation of
cyclin D1 promoter by the ER
Castro-Rivera et al., J Biol Chem 2001
(Breast Neoplasms) :
These results contrasted to a recent report showing that induction of
cyclin D1 by E2 in ER-positive MCF-7 and HeLa cells was
due to up-regulation of c-jun and subsequent interaction of
c-Jun-ATF-2 with the CRE
Zhao et al., Biochem Biophys Res Commun 2002
(Liver Cirrhosis, Experimental) :
In conclusion, downregulation of
cyclin -D1 , -E, and -A expression, which may be
induced by impaired activities of C/EBP and
AP-1 , is responsible for the decreased regenerative capacity of cirrhotic liver after partial hepatectomy
García-Trevijano et al., Gastroenterology 2002
:
Accordingly, we found that S-adenosylmethionine inhibits hepatocyte growth factor induced
cyclin D1 and D2 expression,
activator protein 1 induction , and hepatocyte proliferation
Kim et al., Mol Cells 2002
:
These results suggest that merlin inhibits abnormal cell proliferation which is activated via Ras by repressing Rb phosphorylation, blocking the increase of the
cyclin D1 protein level, and
inhibiting the activation of
AP-1- and E2F-1 dependent transcription in NIH3T3 cells
Soh et al., J Biol Chem 2003
:
A dominant negative mutant of c-Jun inhibited activation of the cyclin D1 promoter in a concentration dependent manner, providing further evidence that
AP-1 activity is
required for activation of the
cyclin D1 promoter by PKC-alpha and PKC-epsilon
Shiozawa et al., Oncogene 2004
:
Estrogen induced proliferation of normal endometrial glandular cells is initiated by transcriptional
activation of
cyclin D1 via binding of
c-Jun to an AP-1 sequence ... These findings suggest that E2-induced proliferation of normal endometrial glandular cells is initiated by transcriptional
activation of
cyclin D1 via binding of
c-Jun to the AP-1 sequences
Chu et al., J Biol Chem 2005
(MAP Kinase Signaling System) :
AP-1 is
required for activation of the
cyclin D1 promoter
Kim et al., J Environ Pathol Toxicol Oncol 2005
(Cell Transformation, Neoplastic) :
We concluded that the inhibitory effect of eupatilin on p21waf1/Cip1 expression is likely to be associated with the downregulation of
cyclin D1 expression and
AP-1 activation , which play an important role in the cell cycle arrest of ras transformed breast epithelial cells
Yao et al., Mol Carcinog 2006
(Urinary Bladder Neoplasms) :
Unexpectedly, neither TAM67 or JNK inhibition, nor forced c-jun expression had a significant impact on cyclin D1 induction by PEITC, indicating that
c-jun/AP-1 does not
play an important role in
cyclin D1 induction by PEITC
Chang et al., Cell Microbiol 2006
(Helicobacter Infections) :
AP1 and cAMP response element ( CRE ), but not NF-kappaB, were
involved in the induced
cyclin D1 expression
Tsuchiya et al., Oncogene 2007
:
Although phosphorylation of c-Jun at Ser-63 is required for
activator protein 1 (AP-1) dependent expression of
cyclin D1 , it decreased in LMB treated cells compared to untreated cells
Ranjan et al., Antioxid Redox Signal 2006
:
In mouse lung epithelial cells that express Nox1, Nox2, Nox4, p22(phox), p47(phox), p67(phox), and Noxo1, overexpression of Nox1 delayed cell cycle withdrawal by maintaining
AP-1 dependent expression of
cyclin D1 in low serum conditions
Li et al., Cancer Res 2006
(Breast Neoplasms) :
The derivatives that stably express the constitutively activated mutants of PKCbeta1 or beta2 also displayed increased
cyclin D1 promoter activity in transient transfection luciferase reporter assays, and this induction of activity
requires activator protein 1
Hao et al., Int J Cancer 2007
(Breast Neoplasms) :
BRCA1-IRIS alone or in complex with steroid receptor co-activators was
targeted to the
cyclin D1 promoter pre bound by the
c-Jun/AP1 and activated its transcription, which could explain the co-overexpression of BRCA1-IRIS and Cyclin D1 in breast cancer cells coupled with their increased proliferation
Lopez-Bergami et al., Cancer Cell 2007
(MAP Kinase Signaling System...) :
Activated
c-Jun is also
responsible for elevated
cyclin D1 expression, which is frequently overexpressed in human melanoma
Zhang et al., Toxicol Appl Pharmacol 2009
:
Collectively, our results demonstrate that
c-Jun/AP-1 mediated
cyclin D1 expression is at least one of the key events implicated in cell transformation upon low dose arsenite exposure
Ding et al., Curr Cancer Drug Targets 2009
:
The inhibition of JNKs or
c-Jun by chemical or genetic inhibitors
blocks the
cyclin D1 induction mediated by arsenite
Naderi et al., Molecular cancer 2010
(Breast Neoplasms) :
Furthermore, using c-Jun stable lines we showed that BEX2 expression is required for
c-Jun mediated induction of
cyclin D1 and cell proliferation
Li et al., Int J Mol Med 2010
:
Pre-treatment of NS3 protein expressing cells with ERK inhibitor, PD98059, blocked the activation of
AP-1 and NF-kappaB, and
inhibited cyclin D1 expression and cell proliferation
Li et al., Toxicol Lett 2011
(Cell Transformation, Neoplastic...) :
Up-regulation of
cyclin D1 by
JNK1/c-Jun is involved in tumorigenesis of human embryo lung fibroblast cells induced by a low concentration of arsenite
Ming et al., Cancer Immunol Immunother 2012
(Carcinoma, Non-Small-Cell Lung...) :
We found that, in lung cancer cell lines and in nude mice, Interleukin-7/Interleukin-7 receptor increased the expression of cyclin D1 and phosphorylation of c-Fos/c-Jun,
induce c-Fos and
c-Jun heterodimer formation, and enhanced c-Fos/c-Jun DNA binding activity to regulate
cyclin D1
Guo et al., Am J Physiol Gastrointest Liver Physiol 2012
:
Chemical inhibitors of JNK and ERK pathways, dominant negative JNK and
c-Jun , and c-Jun shRNA significantly
inhibited CCK induced DNA synthesis, CCK induced AP-1 activation, and
cyclin D1 expression
Zhang et al., BMC cancer 2012
(Carcinoma...) :
BLU inhibits clonogenic growth of nasopharyngeal carcinoma cells, arrests cell cycle at G1 phase, downregulates JNK and
cyclin D1 promoter activities, and
inhibits phosphorylation of
c-Jun
Albanese et al., J Biol Chem 1995
:
The AP-1-like sequences were also required for
activation of the
cyclin D1 promoter by
c-Jun
Kreuzer et al., Free Radic Biol Med 1998
:
The Fos protein forms the heterodimer
AP-1 with the Jun protein and
regulates the cell cycle by inducing
cyclin D1