Neuronal and glioma-derived stem cell factor induces angiogenesis within the brain.

@article{Sun2006NeuronalAG,
  title={Neuronal and glioma-derived stem cell factor induces angiogenesis within the brain.},
  author={Lixin Sun and Aimin Hui and Qin Su and Alexander O. Vortmeyer and Yuri Kotliarov and Sandra Pastorino and Antonino Passaniti and Jayant P. Menon and Jennifer Walling and Rolando Bailey and Marc K. Rosenblum and Tom Mikkelsen and Howard A. Fine},
  journal={Cancer cell},
  year={2006},
  volume={9 4},
  pages={
          287-300
        }
}
Stem cell factor (SCF) is overexpressed by neurons following brain injury as well as by glioma cells; however, its role in gliomagenesis remains unclear. Here, we demonstrate that SCF directly activates brain microvascular endothelial cells (ECs) in vitro and induces a potent angiogenic response in vivo. Primary human gliomas express SCF in a grade-dependent manner and induce normal neurons to express SCF in brain regions infiltrated by glioma cells, areas that colocalize with prominent… Expand
A perivascular niche for brain tumor stem cells.
TLDR
This work shows that endothelial cells interact closely with self-renewing brain tumor cells and secrete factors that maintain these cells in a stem cell-like state, and proposes that brain CSCs are maintained within vascular niches that are important targets for therapeutic approaches. Expand
MEF promotes stemness in the pathogenesis of gliomas.
TLDR
It is found that MEF is highly expressed in both human and mouse glioblastomas and its absence impairs gliomagenesis in a PDGF-driven glioma mouse model, and Sox2 is identified as a direct downstream target of MEF. Expand
Cadherin-11 Regulates Motility in Normal Cortical Neural Precursors and Glioblastoma
TLDR
Findings show that Cadherin-11 can promote cell migration in neural precursors and glioblastoma cells and suggest that endothelial cells increase tumor aggressiveness by co-opting mechanisms that regulate normal neural development. Expand
Dishevelled 2 signaling promotes self-renewal and tumorigenicity in human gliomas.
TLDR
It is shown that Dishevelled 2 (Dvl2), a key component of the Wnt signaling pathway, is overexpressed in human gliomas and RNA interference-mediated depletion of Dvl2 blocked proliferation and promoted the differentiation of cultured humanglioma cell lines and primary, patient-derived glioma cells. Expand
Nodal promotes growth and invasion in human gliomas
TLDR
The data support the notion that Nodal may regulate glioma progression through the induction of the leukemia inhibitory factor (LIF) and Cripto-1 through activated Smad. Expand
Common Denominators of Self-renewal and Malignancy in Neural Stem Cells and Glioma
TLDR
Novel molecular classification of glioblastoma gives hope for more stratified treatment, and the authors are hopefully on the threshold to patient-specific treatments which may finally change the outcome in this devastating disease. Expand
Mast Cell Accumulation in Glioblastoma with a Potential Role for Stem Cell Factor and Chemokine CXCL12
TLDR
It is reported for the first time that MCs infiltrate KRas+Akt-induced gliomas, using the RCAS/TV-a system, where KRas and Akt are transduced by RCAS into the brains of neonatal Gtv-a- or Ntv- a transgenic mice lacking Ink4a or Arf, providing the first evidence for a role for MCs in glioma. Expand
Cadherin-11, a Marker of the Mesenchymal Phenotype, Regulates Glioblastoma Cell Migration and Survival In Vivo
TLDR
The studies suggest cadherin-11 is a viable molecular target for therapeutic intervention in GBM and provide evidence for a novel role of cadherIn-11 in promoting glioma cell survival in an in vivo environment. Expand
KIT overexpression induces proliferation in astrocytes in an imatinib‐responsive manner and associates with proliferation index in gliomas
TLDR
Results indicate that overexpression of KIT in mouse astrocytes promotes cell proliferation, and the increased proliferation is partly inhibited by imatinib treatment, suggesting that KIT may play a role inAstrocyte growth regulation. Expand
The Emerging Role of Myeloid-Derived Suppressor Cells in the Glioma Immune Suppressive Microenvironment
TLDR
Insight into the roles of MDSC immunosuppression in the glioma microenvironment is provided and it is suggested that MDSCs control is a powerful cellular therapeutic target for currently incurable gliomas. Expand
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 65 REFERENCES
Angiogenesis in malignant gliomas
TLDR
A paracrine control of angiogenesis and endothelial cell proliferation that is tightly regulated and transient in the embryonic brain, switched off in the normal adult brain, and turned on in tumor cells (VEGF) and the host vasculature (VEGFR‐1 and −2) during tumor progression is suggested. Expand
Vascular endothelial growth factor is a potential tumour angiogenesis factor in human gliomas in vivo
TLDR
It is shown that expression of an endothelial cell-specific mitogen, vascular endothelial growth factor (VEGF), is induced in astrocytoma cells but is dramatically upregulated in two apparently different subsets of glioblastoma cells, which strongly support the concept that tumour angiogenesis is regulated by paracrine mechanisms and identify VEGF as a potential tumourAngiogenesis factor in vivo. Expand
Anti-angiogenic gene therapy of malignant glioma.
TLDR
Several experimental approaches demonstrate that in rat gliomas tumour growth can be prevented by the inhibition of angiogenesis, of pivotal importance for the development of anti-angiogenic therapies in glioblastoma patients. Expand
Expression of endothelial cell-specific receptor tyrosine kinases and growth factors in human brain tumors.
TLDR
The results are consistent with the hypothesis that these endothelial receptors are induced during tumor progression and may play a role in tumor angiogenesis. Expand
Expression of stem cell factor and c-kit receptor in neural cells after brain injury
TLDR
It is demonstrated that SCF/c-kitR signaling also takes place in situ in the central nervous system, and microglia activated by injury up-regulated c-KitR expression, whereas some astrocytes in the vicinity of the wound expressed SCF mRNA in addition to neurons. Expand
Neuronally expressed stem cell factor induces neural stem cell migration to areas of brain injury.
TLDR
The data suggest that the SCF/c-kit pathway is involved in the migration of NSPCs to sites of brain injury and that SCF may prove useful for inducing progenitor cell recruitment to specific areas of the CNS for cell-based therapeutic strategies. Expand
Modulation of tumor angiogenesis by stem cell factor.
TLDR
Data suggest that SCF modulates tumor growth and angiogenesis via the involvement of mast cells through manipulation of its level in mammary tumors. Expand
Stem cell factor stimulates neurogenesis in vitro and in vivo.
TLDR
Cerebral hypoxia and ischemia may stimulate neurogenesis through trophic factors, including SCF, and in vivo administration of SCF increased BrdU labeling of immature neurons in these regions. Expand
Angiogenesis-related growth factors in brain tumors.
TLDR
The expression pattern of these factors in gliomas, their functional contribution to tumor angiogenesis - also in relation to vascular endothelial growth factor, and the effects resulting from their inhibition or overexpression ingliomas in vivo are reviewed. Expand
Vascular Endothelial Growth Factor-driven Glioma Growth and Vascularization in an Orthotopic Rat Model Monitored by Magnetic Resonance Imaging
TLDR
This model elucidates glioma growth and vascularization as strongly VEGF dependent, which is consistent with human gliomas, and is suitable for testing antiangiogenic strategies to interfere with the V EGF/VEGF receptor system, as well as for exploring VEGf-independent mechanisms using the antisense-transfected clone. Expand
...
1
2
3
4
5
...