Evidence map›Paper›PMID 16995838›Full record

ArticleThe Biochemical journal2007

Clustering of monosialyl-Gb5 initiates downstream signalling events leading to invasion of MCF-7 breast cancer cells.

Severine Van Slambrouck, Wim F A Steelant

Open access · bronzeAbstract read
In one paragraph

Article in The Biochemical journal, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.0field-weighted citation impact, top 27% 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

16 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Increased expression of SSEA-4 on TKI-resistant non-small cell lung cancer with EGFR-T790M mutation.Proceedings of the National Academy of Sciences of the United States of America · 2024
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  8. Signaling pathway of globo-series glycosphingolipids and β1,3-galactosyltransferase V (β3GalT5) in breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
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  12. Stage-specific embryonic antigen-4 as a potential therapeutic target in glioblastoma multiforme and other cancers.Proceedings of the National Academy of Sciences of the United States of America · 2014
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  14. Review
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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

2 authors at 1 institution in 1 country.

Severine Van SlambrouckLaboratory of Biochemical and Biomedical Research, Department of Chemistry, New Mexico Tech, 801 Leroy Place, Socorro, NM 87801, USA.
Wim F A Steelant
New Mexico Institute of Mining and Technology · US

Funding

ZUNI HEALTH INITIATIVE-PILOT STUDYP20RR016480 · NCRR · NEW MEXICO STATE UNIVERSITY LAS CRUCES · PI ZHANG, PENG F · 2001 to 2011
$33.7M
NCRR NIH HHS P20 RR016480NCRR NIH HHS RR-16480
6 · The paper itself

Abstract

Invasion is a complex process controlled by secretion and activation of proteases, alteration of integrin levels and GSL (glycosphingolipid) patterns. Differential organization of GSLs with specific membrane proteins and signal transducers in GEMs (GSL-enriched microdomains), initiates signalling events to modify cellular phenotype. Although the GSL monosialyl-Gb5 has been linked with invasion, its functional role in invasion is poorly described and understood. To investigate this problem, we induced the invasion of human breast cancer cells and subsequently explored the underlying mechanism. In the present study, the invasion of human MCF-7 breast cancer cells is highly dependent on clustering of monosialyl-Gb5, and the subsequent activation of monosialyl-Gb5-associated focal adhesion kinase and cSrc in GEM leading to the downstream activation of extracellular-signal-regulated kinase (ERK). As a result, we observed increased expression levels and activity of matrix metalloproteinases-2 and -9, which correlated with decreased expression of integrins alpha1 and beta1. Together these results suggest that the organization of crucial molecules in GEMs of MCF-7 cells is critical for their invasive properties.

Indexed as

Signal TransductionBreast NeoplasmsCell Line, TumorExtracellular Signal-Regulated MAP KinasesFemaleFocal Adhesion Kinase 1Gene Expression Regulation, NeoplasticGlycosphingolipidsHumansIntegrinsMatrix MetalloproteinasesMembrane MicrodomainsNeoplasm InvasivenessPhosphatidylcholinesPhospholipid EthersedelfosineExtracellular Signal-Regulated MAP KinasesFocal Adhesion Kinase 1GlycosphingolipidsIntegrinsMatrix MetalloproteinasesPhosphatidylcholinesPhospholipid EthersPTK2 protein, human

Identifiers

PMID16995838
PMCPMC1770852
OpenAlexW1977818746

What OpenQuestion holds

Textmetadata
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.