Evidence map›Paper›PMID 18794124›Full record

ArticleCancer research2008

An immortalization-dependent switch in integrin function up-regulates MMP-9 to enhance tumor cell invasion.

John M Lamar, Kevin M Pumiglia, C Michael DiPersio

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.6field-weighted citation impact, top 14% 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

30 citing papers in PubMed, 49 citations in OpenAlex.

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  19. Loss of integrin α3 prevents skin tumor formation by promoting epidermal turnover and depletion of slow-cycling cells.Proceedings of the National Academy of Sciences of the United States of America · 2012
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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

3 authors at 1 institution in 1 country.

John M LamarCenter for Cell Biology and Cancer Research, Albany Medical College, Albany, New York 12208-3479, USA.
Kevin M Pumiglia
C Michael DiPersio
Albany Medical Center Hospital · US

Funding

TISSUE REMODELING AND CARDIOVASCULAR DISEASET32HL007194 · NHLBI · ALBANY MEDICAL COLLEGE · PI MC KEOWN-LONGO, PAULA J · 1985 to 2006
$2.9M
VEGF SIGNAL TRANSDUCTION AND TUMOR ANGIOGENESISR01CA081419 · NCI · ALBANY MEDICAL COLLEGE · PI PUMIGLIA, KEVIN M · 1999 to 2008
$2.0M
CONTROL OF MATRIX PROTEOLYSIS BY INTEGRIN A3B1 IN SKINR01CA084238 · NCI · ALBANY MEDICAL COLLEGE · PI DIPERSIO, C MICHAEL · 2000 to 2005
$951k
NCI NIH HHS R01 CA081419NCI NIH HHS R01 CA084238NCI NIH HHS R01CA81419NCI NIH HHS R01CA84238NHLBI NIH HHS T32 HL007194NHLBI NIH HHS T32-HL-07194
6 · The paper itself

Abstract

Integrins, the major receptors for cell adhesion to the extracellular matrix, play important roles during tumor progression. However, it is still unclear whether genetic lesions that occur during carcinoma development can lead to altered integrin function, and how changes in integrin function contribute to subsequent carcinoma progression. Loss-of-function mutations in p53 and activating mutations in H-Ras, which immortalize and transform epithelial cells, respectively, are common causal events in squamous cell carcinoma (SCC). Phenotypes resulting from these two genetic lesions promote SCC progression and are, therefore, potential targets for anticancer therapies. We developed a model system of keratinocyte transformation that has allowed us to investigate the individual roles of p53 mutation and oncogenic Ras mutation in the acquisition of integrin alpha3beta1-regulated phenotypes that promote SCC progression. Using this model, we show that keratinocyte immortalization by p53-null mutation causes a switch in alpha3beta1 function that induces matrix metalloproteinase (MMP)-9 gene expression in tumorigenic cells. This acquired alpha3beta1-dependent regulation of MMP-9 was maintained during subsequent transformation by oncogenic Ras, and it promoted invasion of tumorigenic keratinocytes. Our results show that loss of p53 function leads to changes in integrin-mediated gene regulation that occur during SCC progression and play a critical role in tumor cell invasion.

Indexed as

AnimalsCarcinoma, Squamous CellCell Line, TransformedCells, CulturedCell Transformation, NeoplasticGene ExpressionHumansIntegrin alpha3beta1KeratinocytesMatrix Metalloproteinase 9MiceMice, NudeNeoplasm InvasivenessRNA, MessengerTumor Suppressor Protein p53Up-RegulationIntegrin alpha3beta1Matrix Metalloproteinase 9RNA, MessengerTumor Suppressor Protein p53

Identifiers

PMID18794124
PMCPMC2782775
OpenAlexW2116672575

What OpenQuestion holds

Textmetadata
LicenceTDM
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.