1
40
3
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1038/sj.onc.1207774" target="_blank" rel="noreferrer noopener">http://doi.org/10.1038/sj.onc.1207774</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
5858-5863
Issue
34
Volume
23
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Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
The Ras-related protein AGS1/RASD1 suppresses cell growth
Publisher
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Oncogene
Date
A point or period of time associated with an event in the lifecycle of the resource
2004
2004-07
Subject
The topic of the resource
activation; AGS1; apoptosis; binding protein; Biochemistry & Molecular Biology; cancer; Cell Biology; coupled receptors; Dexras1; Dexras1; G protein; gene; Genetics &; Heredity; hormone; identification; Integration; Oncology; RASD1; signal-transduction
Creator
An entity primarily responsible for making the resource
Vaidyanathan G; Cismowski M J; Wang G S; Vincent T S; Brown K D; Lanier S M
Description
An account of the resource
AGS1/RASD1 is a Ras-related protein identified as a dexamethasone-inducible cDNA and as a signal regulator in various functional and protein-interaction screens. As an initial approach to define the role of AGS1/RASD1 as a Ras-family member, we determined its influence on cell growth/survival. In clonogenic assays with NIH-3T3 murine fibroblast cells, the MCF-7 human breast cancer cell line and the human lung adenocarcinoma cell line A549, AGS1/RASD1 markedly diminished the number of G418-resistant colonies, whereas the Ras subgroup member K-Ras was without effect. A549 cell infection with adenovirus engineered to express AGS1/RASD1 (Ad.AGS1) inhibited log phase growth in vitro and increased the percentage of cells undergoing apoptosis. The anti-growth action was also observed in vivo as the expression of AGS1/RASD1 inhibited the subcutaneous tumor growth of A549 cells in athymic nude mice. These data indicate that AGS1/RASD1, a member of the Ras superfamily of small G-proteins that often promotes cell growth and tumor expansion, plays an active role in preventing aberrant cell growth.
Identifier
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<a href="http://doi.org/10.1038/sj.onc.1207774" target="_blank" rel="noreferrer noopener">10.1038/sj.onc.1207774</a>
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Journal Article
2004
activation
AGS1
Apoptosis
binding protein
Biochemistry & Molecular Biology
Brown K D
Cancer
Cell Biology
Cismowski M J
coupled receptors
Dexras1
G protein
gene
Genetics &
Heredity
hormone
identification
Integration
Journal Article
Lanier S M
Oncogene
oncology
RASD1
signal-transduction
Vaidyanathan G
Vincent T S
Wang G S
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1038/onc.2017.140" target="_blank" rel="noreferrer noopener">http://doi.org/10.1038/onc.2017.140</a>
Pages
5189–5198
Issue
36
Volume
36
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Thrombospondin-4 mediates TGF-beta-induced angiogenesis.
Publisher
An entity responsible for making the resource available
Oncogene
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-09
Subject
The topic of the resource
Angiogenesis Inducing Agents/*metabolism; Animals; Cell Movement/drug effects; Cell Proliferation/drug effects; Cells; Chick Embryo; Cultured; Endothelium; Female; Gene Expression Regulation/drug effects; Humans; Inbred C57BL; Male; Mice; Muscle; Neovascularization; Pathologic/drug therapy/metabolism/*pathology; Signal Transduction/drug effects; Smooth; Thrombospondins/*physiology; Transforming Growth Factor beta/*pharmacology; Vascular/drug effects/metabolism/*pathology
Creator
An entity primarily responsible for making the resource
Muppala S; Xiao R; Krukovets I; Verbovetsky D; Yendamuri R; Habib N; Raman P; Plow E; Stenina-Adognravi O
Description
An account of the resource
TGF-beta is a multifunctional cytokine affecting many cell types and implicated in tissue remodeling processes. Due to its many functions and cell-specific effects, the consequences of TGF-beta signaling are process-and stage-dependent, and it is not uncommon that TGF-beta exerts distinct and sometimes opposing effects on a disease progression depending on the stage and on the pathological changes associated with the stage. The mechanisms underlying cell- and process-specific effects of TGF-beta are poorly understood. We are describing a novel pathway that mediates induction of angiogenesis in response to TGF-beta1. We found that in endothelial cells (EC) thrombospondin-4 (TSP-4), a secreted extracellular matrix (ECM) protein, is upregulated in response to TGF-beta1 and mediates the effects of TGF-beta1 on angiogenesis. Upregulation of TSP-4 does not require the synthesis of new protein, is not caused by decreased secretion of
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1038/onc.2017.140" target="_blank" rel="noreferrer noopener">10.1038/onc.2017.140</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2017
Angiogenesis Inducing Agents/*metabolism
Animals
Cell Movement/drug effects
Cell Proliferation/drug effects
Cells
Chick Embryo
Cultured
Department of Integrative Medical Sciences
Endothelium
Female
Gene Expression Regulation/drug effects
Habib N
Humans
Inbred C57BL
Krukovets I
Male
Mice
Muppala S
Muscle
NEOMED College of Medicine
Neovascularization
Oncogene
Pathologic/drug therapy/metabolism/*pathology
Plow E
Raman P
Signal Transduction/drug effects
Smooth
Stenina-Adognravi O
Thrombospondins/*physiology
Transforming Growth Factor beta/*pharmacology
Vascular/drug effects/metabolism/*pathology
Verbovetsky D
Xiao R
Yendamuri R
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1038/onc.2015.83" target="_blank" rel="noreferrer noopener">http://doi.org/10.1038/onc.2015.83</a>
Pages
314–322
Issue
3
Volume
35
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Activation of mechanosensitive ion channel TRPV4 normalizes tumor vasculature and improves cancer therapy.
Publisher
An entity responsible for making the resource available
Oncogene
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-01
Subject
The topic of the resource
Animals; Calcium Signaling/genetics; Carcinoma; Cell Line; Cell Proliferation/drug effects; Cisplatin/administration & dosage; Endothelium; Gene Expression Regulation; Humans; Leucine/administration & dosage/analogs & derivatives; Lewis Lung/drug therapy/*genetics/pathology; Mice; Neoplastic/drug effects; Neovascularization; Pathologic/drug therapy/*genetics/pathology; Sulfonamides/administration & dosage; TRPV Cation Channels/agonists/biosynthesis/*genetics; Tumor; Vascular Endothelial Growth Factor A/genetics; Vascular/drug effects/*pathology
Creator
An entity primarily responsible for making the resource
Adapala R K; Thoppil R J; Ghosh K; Cappelli H C; Dudley A C; Paruchuri S; Keshamouni V; Klagsbrun M; Meszaros J G; Chilian W M; Ingber D E; Thodeti C K
Description
An account of the resource
Tumor vessels are characterized by abnormal morphology and hyperpermeability that together cause inefficient delivery of chemotherapeutic agents. Although vascular endothelial growth factor has been established as a critical regulator of tumor angiogenesis, the role of mechanical signaling in the regulation of tumor vasculature or tumor endothelial cell (TEC) function is not known. Here we show that the mechanosensitive ion channel transient receptor potential vanilloid 4 (TRPV4) regulates tumor angiogenesis and tumor vessel maturation via modulation of TEC mechanosensitivity. We found that TECs exhibit reduced TRPV4 expression and function, which is correlated with aberrant mechanosensitivity towards extracellular matrix stiffness, increased migration and abnormal angiogenesis by TEC. Further, syngeneic tumor experiments revealed that the absence of TRPV4 induced increased vascular density, vessel diameter and reduced pericyte coverage resulting in enhanced tumor growth in TRPV4 knockout mice. Importantly, overexpression or pharmacological activation of TRPV4 restored aberrant TEC mechanosensitivity, migration and normalized abnormal angiogenesis in vitro by modulating Rho activity. Finally, a small molecule activator of TRPV4, GSK1016790A, in combination with anticancer drug cisplatin, significantly reduced tumor growth in wild-type mice by inducing vessel maturation. Our findings demonstrate TRPV4 channels to be critical regulators of tumor angiogenesis and represent a novel target for anti-angiogenic and vascular normalization therapies.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1038/onc.2015.83" target="_blank" rel="noreferrer noopener">10.1038/onc.2015.83</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2016
Adapala R K
Animals
Calcium Signaling/genetics
Cappelli H C
Carcinoma
Cell Line
Cell Proliferation/drug effects
Chilian W M
Cisplatin/administration & dosage
Department of Integrative Medical Sciences
Dudley A C
Endothelium
Gene Expression Regulation
Ghosh K
Humans
Ingber D E
Keshamouni V
Klagsbrun M
Leucine/administration & dosage/analogs & derivatives
Lewis Lung/drug therapy/*genetics/pathology
Meszaros J G
Mice
NEOMED College of Medicine
Neoplastic/drug effects
Neovascularization
Oncogene
Paruchuri S
Pathologic/drug therapy/*genetics/pathology
Sulfonamides/administration & dosage
Thodeti C K
Thoppil R J
TRPV Cation Channels/agonists/biosynthesis/*genetics
Tumor
Vascular Endothelial Growth Factor A/genetics
Vascular/drug effects/*pathology