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Text
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URL Address
<a href="http://doi.org/10.1002/jcp.25279" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/jcp.25279</a>
Pages
1761–1770
Issue
8
Volume
231
Dublin Core
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Title
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Osteoactivin Promotes Migration of Oral Squamous Cell Carcinomas.
Publisher
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Journal of cellular physiology
Date
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2016
2016-08
Subject
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*Cell Movement; Carcinoma; Cell Adhesion; Cell Line; Cell Proliferation; Cell Survival; Enzyme Activation; Gene Expression Regulation; Head and Neck Neoplasms/genetics/*metabolism/pathology; Humans; Integrin beta1/metabolism; Membrane Glycoproteins/genetics/*metabolism; Messenger/metabolism; Mitogen-Activated Protein Kinases/metabolism; Mouth Neoplasms/genetics/*metabolism/pathology; Neoplasm Invasiveness; Neoplastic; Protein Binding; RNA; RNA Interference; Signal Transduction; Squamous Cell Carcinoma of Head and Neck; Squamous Cell/genetics/*metabolism/pathology; Time Factors; Transfection; Tumor
Creator
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Arosarena Oneida A; Dela Cadena Raul A; Denny Michael F; Bryant Evan; Barr Eric W; Thorpe Ryan; Safadi Fayez F
Description
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Nearly 50% of patients with oral squamous cell carcinoma (OSCC) die of metastases or locoregional recurrence. Metastasis is mediated by cancer cell adhesion, migration, and invasion. Osteoactivin (OA) overexpression plays a role in metastases in several malignancies. The aims were to determine how integrin interactions modulate OA-induced OSCC cell migration; and to investigate OA effects on cell survival and proliferation. We confirmed OA mRNA and protein overexpression in OSCC cell lines. We assessed OA's interactions with integrins using adhesion inhibition assays, fluorescent immunocytochemistry and co-immunoprecipitation. We investigated OA-mediated activation of mitogen-activated protein kinases (MAPKs) and cell survival. Integrin inhibition effects on OA-mediated cell migration were determined. We assessed effects of OA knock-down on cell migration and proliferation. OA is overexpressed in OSCC cell lines, and serves as a migration-promoting adhesion molecule. OA co-localized with integrin subunits, and co-immunoprecipitated with the subunits. Integrin blocking antibodies, especially those directed against the beta1 subunit, inhibited cell adhesion (P = 0.03 for SCC15 cells). Adhesion to OA activated MAPKs in UMSCC14a cells and OA treatment promoted survival of SCC15 cells. Integrin-neutralizing antibodies enhanced cell migration with OA in the extracellular matrix. OA knock-down resulted in decreased proliferation of SCC15 and SCC25 cells, but did not inhibit cell migration. OA in the extracellular matrix promotes OSCC cell adhesion and migration, and may be a novel target in the prevention of HNSCC spread. J. Cell. Physiol. 231: 1761-1770, 2016. (c) 2015 Wiley Periodicals, Inc.
Identifier
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<a href="http://doi.org/10.1002/jcp.25279" target="_blank" rel="noreferrer noopener">10.1002/jcp.25279</a>
Rights
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Cell Movement
2016
Arosarena Oneida A
Barr Eric W
Bryant Evan
Carcinoma
Cell Adhesion
Cell Line
Cell Proliferation
Cell Survival
Dela Cadena Raul A
Denny Michael F
Department of Anatomy & Neurobiology
Enzyme Activation
Gene Expression Regulation
Head and Neck Neoplasms/genetics/*metabolism/pathology
Humans
Integrin beta1/metabolism
Journal of cellular physiology
Membrane Glycoproteins/genetics/*metabolism
Messenger/metabolism
Mitogen-Activated Protein Kinases/metabolism
Mouth Neoplasms/genetics/*metabolism/pathology
NEOMED College of Medicine
Neoplasm Invasiveness
Neoplastic
Protein Binding
RNA
RNA Interference
Safadi Fayez F
Signal Transduction
Squamous Cell Carcinoma of Head and Neck
Squamous Cell/genetics/*metabolism/pathology
Thorpe Ryan
Time Factors
Transfection
Tumor