Alternatively spliced FGFR-1 isoforms differentially modulate endothelial cell activation of c-YES

Zhang, Pei; Greendorfer, Jessica S; Jiao, Jing; Kelpke, Stacey C.; Thompson, John A.

doi:10.1016/j.abb.2006.03.017

Cited by 19 publications

(13 citation statements)

References 58 publications

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“…FGF-1 induces growth arrest and differentiation in chondrocytes [89–92]. It is implicated in angiogenesis [93–95] and wound healing [95–99]. Multiple studies have also shown the role of FGF-1 in cardioprotection [99–101] and neuroprotection [22, 102].…”

Section: Resultsmentioning

confidence: 99%

A Network Map of FGF-1/FGFR Signaling System

Raju

Palapetta

Sandhya

et al. 2014

Journal of Signal Transduction

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Fibroblast growth factor-1 (FGF-1) is a well characterized growth factor among the 22 members of the FGF superfamily in humans. It binds to all the four known FGF receptors and regulates a plethora of functions including cell growth, proliferation, migration, differentiation, and survival in different cell types. FGF-1 is involved in the regulation of diverse physiological processes such as development, angiogenesis, wound healing, adipogenesis, and neurogenesis. Deregulation of FGF-1 signaling is not only implicated in tumorigenesis but also is associated with tumor invasion and metastasis. Given the biomedical significance of FGFs and the fact that individual FGFs have different roles in diverse physiological processes, the analysis of signaling pathways induced by the binding of specific FGFs to their cognate receptors demands more focused efforts. Currently, there are no resources in the public domain that facilitate the analysis of signaling pathways induced by individual FGFs in the FGF/FGFR signaling system. Towards this, we have developed a resource of signaling reactions triggered by FGF-1/FGFR system in various cell types/tissues. The pathway data and the reaction map are made available for download in different community standard data exchange formats through NetPath and NetSlim signaling pathway resources.

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Section: Resultsmentioning

confidence: 99%

A Network Map of FGF-1/FGFR Signaling System

Raju

Palapetta

Sandhya

et al. 2014

Journal of Signal Transduction

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“…These truncated soluble EGFR variants have been detected in several cancer types, and their levels, circulating as well as in tumor tissues, have been used as prognostic and predictive markers for ovarian, cervical, lung, and breast cancers [57–59]. Alternative splicing of other tyrosine kinase receptors such as the insulin, IGF-1, FGF, ERBB2, and ERBB4 receptors can also modulate the activation of their downstream signalling pathways [2, 19, 29, 36, 60–65]. An additional example of alternative splicing in the Ras-MAPK pathway is the splicing of MEK1b and ERK1c [66, 67].…”

Section: Regulation Of the Ras-mapk Pathway By Alternative Splicingmentioning

confidence: 99%

Regulation of the Ras-MAPK and PI3K-mTOR Signalling Pathways by Alternative Splicing in Cancer

Siegfried¹,

Bonomi

Ghigna

et al. 2013

International Journal of Cell Biology

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Alternative splicing is a fundamental step in regulation of gene expression of many tumor suppressors and oncogenes in cancer. Signalling through the Ras-MAPK and PI3K-mTOR pathways is misregulated and hyperactivated in most types of cancer. However, the regulation of the Ras-MAPK and PI3K-mTOR signalling pathways by alternative splicing is less well established. Recent studies have shown the contribution of alternative splicing regulation of these signalling pathways which can lead to cellular transformation, cancer development, and tumor maintenance. This review will discuss findings in the literature which describe new modes of regulation of components of the Ras-MAPK and PI3K-mTOR signalling pathways by alternative splicing. We will also describe the mechanisms by which signals from extracellular stimuli can be communicated to the splicing machinery and to specific RNA-binding proteins that ultimately control exon definition events.

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“…It is possible that individual VEGFR1 isoforms have unique signaling patterns as it has been reported for FGFR1, a closely related tyrosine kinase receptor. 30 This could explain (at least in part) the differences in response to endothelial cell-secreted factors that were observed here.…”

Section: Discussionmentioning

confidence: 78%

Endothelial derived factors inhibit anoikis of head and neck cancer stem cells

et al. 2012

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Recent evidence demonstrated that cancer stem cells reside in close proximity to blood vessels in human head and neck squamous cell carcinomas (HNSCC). These findings suggest the existence of a supporting perivascular niche for cancer stem cells. Objective The purpose of this study was to evaluate the effect of endothelial cell-secreted factors on the behavior of head and neck cancer stem-like cells (HNCSC). Materials and methods HNCSC were identified by sorting UM-SCC-22A (cell line derived from a primary squamous cell carcinoma of the oropharynx) and UM-SCC-22B (derived from the metastatic lymph node of the same patient) for CD44 expression and ALDH (aldehyde dehydrogenase) activity. HNCSC (ALDH+CD44+) and control (ALDH−CD44−) cells were cultured in ultra-low attachment plates in presence of conditioned medium from primary human endothelial cells. Results ALDH+CD44+ generated more orospheres than control cells when cultured in suspension. The growth factor milieu secreted by endothelial cells protected HNCSC against anoikis. Mechanistic studies revealed that endothelial cell-secreted vascular endothelial growth factor (VEGF) induces proliferation of HNCSC derived from primary UM-SCC-22A, but not from the metastatic UM-SCC-22B. Likewise, blockade of VEGF abrogated endothelial cell-induced Akt phosphorylation in HNCSC derived from UM-SCC-22A while it had a modest effect in Akt phosphorylation in HNCSC from UM-SCC-22B. Conclusion This study revealed that endothelial cells initiate a crosstalk that protect head and neck cancer stem cells against anoikis, and suggest that therapeutic interference with this crosstalk might be beneficial for patients with head and neck cancer.

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Alternatively spliced FGFR-1 isoforms differentially modulate endothelial cell activation of c-YES

Cited by 19 publications

References 58 publications

A Network Map of FGF-1/FGFR Signaling System

A Network Map of FGF-1/FGFR Signaling System

Regulation of the Ras-MAPK and PI3K-mTOR Signalling Pathways by Alternative Splicing in Cancer

Endothelial derived factors inhibit anoikis of head and neck cancer stem cells

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