Critical role for NF‐κB‐induced JunB in VEGF regulation and tumor angiogenesis

@article{Schmidt2007CriticalRF,
  title={Critical role for NF‐$\kappa$B‐induced JunB in VEGF regulation and tumor angiogenesis},
  author={D. Schmidt and B. Textor and Oliver T. Pein and A. Licht and S. Andrecht and Melanie Sator-Schmitt and N. Fusenig and P. Angel and M. Schorpp-Kistner},
  journal={The EMBO Journal},
  year={2007},
  volume={26}
}
Regulation of vascular endothelial growth factor (VEGF) expression is a complex process involving a plethora of transcriptional regulators. The AP‐1 transcription factor is considered as facilitator of hypoxia‐induced VEGF expression through interaction with hypoxia‐inducible factor (HIF) which plays a major role in mediating the cellular hypoxia response. As yet, both the decisive AP‐1 subunit leading to VEGF induction and the molecular mechanism by which this subunit is activated have not… Expand
Loss of stromal JUNB does not affect tumor growth and angiogenesis
TLDR
It is shown that ablation of Junb in stromal cells including endothelial cells, vascular smooth muscle cells and fibroblasts does not affect tumor growth in two different syngeneic mouse models, the B16‐F1 melanoma and the Lewis lung carcinoma model. Expand
Junb controls lymphatic vascular development in zebrafish via miR-182
TLDR
It is demonstrated that the oncogenic miR-182 is a novel JUNB target and attenuates foxo1 expression indicating that strictly balanced Foxo1 levels are required for proper lymphatic vascular development in zebrafish. Expand
Activating transcription factor 2 increases transactivation and protein stability of hypoxia-inducible factor 1alpha in hepatocytes.
TLDR
Results show that protein stabilization of ATF-2 under hypoxic conditions is required for the induction of the protein stability and transactivation activity of HIF-1alpha for efficient hypoxia-associated gene expression. Expand
Sphingosine 1-Phosphate Receptor Signaling Establishes AP-1 Gradients to Allow for Retinal Endothelial Cell Specialization.
TLDR
It is shown that retinal endothelial sphingosine 1-phosphate receptors (S1PRs), which restrain vascular endothelial growth factor-induced angiogenesis, spatially restrict expression of JunB, a member of the activator protein 1 (AP-1) family of transcription factors (TFs), creating an AP-1 gradient and enabling organotypic endothelial cell specialization of the vascular network. Expand
Roles of NF-κB Signaling in the Regulation of miRNAs Impacting on Inflammation in Cancer
TLDR
It is proposed that studying active TF-miRNA transcriptional regulatory networks such as NF-κB-mi RNA networks in specific cancer types can contribute to the further understanding of the regulatory interplay between inflammation and cancer, and also perhaps lead to the development of pharmacologically novel therapeutic approaches to combat cancer. Expand
Members of the CREB/ATF and AP1 family of transcription factors are involved in the regulation of SOX18 gene expression
TLDR
Functional analysis revealed that CREB acts as a repressor, while JunB, c-Jun and ATF3 act as activators of SOX18 promoter activity, indicating that a transcriptional network that includes CREB, Jun B, c -Jun and ATF3 could be involved in angiogenesis-related transcriptional regulation of the SoX18 gene. Expand
Mechanisms of adaptive angiogenesis to tissue hypoxia
  • G. Fong
  • Biology, Medicine
  • Angiogenesis
  • 2008
TLDR
Five topics are discussed which indicate that while mechanisms of oxygen-regulated HIF-α stability provide exciting opportunities for the development of angiogenesis or anti-angiogenesis therapies, it is also highly important to consider various other mechanisms for the optimization of these procedures. Expand
Tobacco carcinogen mediated up‐regulation of AP‐1 dependent pro‐angiogenic cytokines in head and neck carcinogenesis
TLDR
It is hypothesize that tobacco products may induce microenvironment alterations, promoting angiogenesis and providing a permissive environment for head and neck cancer progression, and conclude tobacco carcinogens up‐regulate AP‐1 activity andAP‐1 dependent IL‐8 and VEGF gene expression in head and head cancer. Expand
JunB is a key regulator of multiple myeloma bone marrow angiogenesis
TLDR
It is revealed for the first time that JunB is not only a mediator of MM cell survival, proliferation, and drug resistance, but also a promoter of AF transcription and consequently of MM BM angiogenesis. Expand
Role of JunB in Adenosine A2B Receptor–Mediated Vascular Endothelial Growth Factor Production
TLDR
An important role is suggested of the A2B receptor-dependent upregulation of JunB in VEGF production and possibly other AP-1–regulated events. Expand
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 68 REFERENCES
c-JUN gene induction and AP-1 activity is regulated by a JNK-dependent pathway in hypoxic HepG2 cells.
TLDR
Results indicate that, in hypoxic HepG2 cells, AP-1 is activated through a JNK-dependent pathway and that it is involved in the regulation of the c-jun promoter, inducing a positive feedback loop on AP- 1 activation via c-Jun overexpression. Expand
JunB is required for endothelial cell morphogenesis by regulating core-binding factor β
TLDR
It is demonstrated that cell-autonomous endothelial functions of the AP-1 subunit JunB are required for proper endothelial morphogenesis both in vivo in mouse embryos with endothelial-specific ablation of JunB and in in vitro angiogenesis models. Expand
IL‐1β mediated up‐regulation of HIF‐lα via an NFkB/COX‐2 pathway identifies HIF‐1 as a critical link between inflammation and oncogenesis
TLDR
It is demonstrated that IL‐1β up‐regulates functional HIF‐1α protein through a classical inflammatory signaling pathway involving NFkB and COX‐2, culminating in up‐regulation of VEGF, a potent angiogenic factor required for tumor growth and metastasis. Expand
The Response of c-Jun/AP-1 to Chronic Hypoxia Is Hypoxia-Inducible Factor 1α Dependent
TLDR
Evidence obtained by using wild-type and HIF-1α nullizygous mouse embryonic fibroblasts that the induction of c-jun mRNA expression and c-Jun phosphorylation are completely dependent on the presence of the oxygen-regulated transcription factor hypoxia-inducible factor 1α is suggested. Expand
c-Jun and Hypoxia-Inducible Factor 1 Functionally Cooperate in Hypoxia-Induced Gene Transcription
TLDR
C-Jun functionally cooperates with HIF-1 transcriptional activity in different cell types and provides a novel insight into the regulation of some genes, such as the one for VEGF, which is a key regulator of tumor angiogenesis. Expand
JunD Reduces Tumor Angiogenesis by Protecting Cells from Oxidative Stress
TLDR
JunD, a member of the AP-1 family of transcription factors, reduces tumor angiogenesis by limiting Ras-mediated production of ROS and provides new insights into the regulation of PHD activity, allowing immediate reactive adaptation to changes in O2 or iron levels in the cell. Expand
Transcriptional regulation of the Vascular Endothelial Growth Factor gene--a concert of activating factors.
TLDR
Two transcription factors essential to VEGF gene transcription are focused on: the hypoxia-inducible factor-1, which is responsible for its increased by Hypoxia, as well as Sp1,which is implicated in the response to various extracellular stimuli. Expand
Activator-protein-1 binding potentiates the hypoxia-induciblefactor-1-mediated hypoxia-induced transcriptional activation of vascular-endothelial growth factor expression in C6 glioma cells.
TLDR
It is reported that the binding site of hypoxia-inducible factor 1 (HIF1) is crucial for the hypoxic induction of VEGF gene expression, however, an enhancer subfragment containing the HIF1 binding site was not sufficient to confer full Hypoxia responsiveness. Expand
IL-1beta-mediated up-regulation of HIF-1alpha via an NFkappaB/COX-2 pathway identifies HIF-1 as a critical link between inflammation and oncogenesis.
TLDR
It is demonstrated that IL-1beta up-regulates functional HIF-1alpha protein through a classical inflammatory signaling pathway involving NFkB and COX-2, culminating in up-regulation of VEGF, a potent angiogenic factor required for tumor growth and metastasis. Expand
Hypoxia-inducible Factor-1α Is a Positive Factor in Solid Tumor Growth
TLDR
The evidence from these experiments indicates that hypoxic response via Hif-1α is an important positive factor in solid tumor growth and that HIF-1 α affects tumor expansion in ways unrelated to its regulation of VEGF expression. Expand
...
1
2
3
4
5
...