Evidence map›Paper›PMID 20579373›Full record

ArticleBMC cancer2010

The CS1 segment of fibronectin is involved in human OSCC pathogenesis by mediating OSCC cell spreading, migration, and invasion.

Pachiyappan Kamarajan, Angeles Garcia-Pardo, Nisha J D'Silva, Yvonne L Kapila

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.3field-weighted citation impact, top 44% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 35 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 2 countries.

Pachiyappan KamarajanDepartment of Periodontics and Oral Medicine, School of Dentistry, University of Michigan, Ann Arbor, Michigan 48109-1078, USA.
Angeles Garcia-Pardo
Nisha J D'Silva
Yvonne L Kapila
University of Michigan–Ann Arbor · USCentro de Investigaciones Biológicas Margarita Salas · ES

Funding

FIBRONECTIN REGULATION OF CARCINOMA APOPTOSISR01DE014429 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KAPILA, YVONNE L · 2004 to 2009
$1.3M
NIDCR NIH HHS R01 DE014429
6 · The paper itself

Abstract

backgroundThe alternatively spliced V region or type III connecting segment III (IIICS) of fibronectin is important in early development, wound healing, and tumorigenesis, however, its role in oral cancer has not been fully investigated. Thus, we investigated the role of CS-1, a key site within the CSIII region of fibronectin, in human oral squamous cell carcinoma (OSCC).

methodsTo determine the expression of CS-1 in human normal and oral SCC tissue specimens immunohistochemical analyses were performed. The expression of CS1 was then associated with clinicopathological factors. To investigate the role of CS-1 in regulating OSCC cell spreading, migration and invasion, OSCC cells were assayed for spreading and migration in the presence of a CS-1 peptide or a CS-1 blocking peptide, and for invasion using Matrigel supplemented with these peptides. In addition, integrin alpha4siRNA or a focal adhesion kinase (FAK) anti-sense oligonucleotide was transfected into OSCC cells to examine the mechanistic role of integrin alpha4 or FAK in CS1-mediated cell spreading and migration, respectively.

resultsCS-1 expression levels were significantly higher in OSCC tissues compared to normal tissues (p < 0.05). Also, although, high levels of CS-1 expression were present in all OSCC tissue samples, low-grade tumors stained more intensely than high grade tumors. OSCC cell lines also expressed higher levels of CS-1 protein compared to normal human primary oral keratinocytes. There was no significant difference in total fibronectin expression between normal and OSCC tissues and cells. Inclusion of CS-1 in the in vitro assays enhanced OSCC cell spreading, migration and invasion, whereas the CS1 blocking peptide inhibited these processes. Suppression of integrin alpha4 significantly inhibited the CS1-mediated cell spreading. Furthermore, this migration was mediated by focal adhesion kinase (FAK), since FAK suppression significantly blocked the CS1-induced cell migration.

conclusionThese data indicate that the CS-1 site of fibronectin is involved in oral cancer pathogenesis and in regulating OSCC cell spreading, migration and invasion.

Indexed as

Cell MovementCell ShapeCarcinoma, Squamous CellCell Line, TumorFibronectinsFocal Adhesion Kinase 1HumansImmunohistochemistryIntegrin alpha4Intercellular Signaling Peptides and ProteinsKeratinocytesMouth NeoplasmsNeoplasm InvasivenessNeoplasm StagingPeptidesRNA InterferenceCS1 peptideFibronectinsFocal Adhesion Kinase 1Integrin alpha4Intercellular Signaling Peptides and ProteinsPeptidesPTK2 protein, human

Identifiers

PMID20579373
PMCPMC3146068
OpenAlexW2004959243

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.