Evidence map›Paper›PMID 16849564›Full record

ArticleCancer research2006

Chemokine (C-C motif) ligand 2 mediates the prometastatic effect of dysadherin in human breast cancer cells.

Jeong-Seok Nam, Mi-Jin Kang, Adam M Suchar, Takeshi Shimamura, Ethan A Kohn, Aleksandra M Michalowska, V Craig Jordan, Setsuo Hirohashi, Lalage M Wakefield

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

69 citing papers in PubMed, 1 synthesis or guideline pooled it, 106 citations in OpenAlex.

  1. Pooled it
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  9. Lung metastases.Nature reviews. Disease primers · 2025
    Review
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9 more citing papers are in PubMed but not listed here.

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

9 authors at 3 institutions in 2 countries.

Jeong-Seok NamLaboratory of Cell Regulation and Carcinogenesis, National Cancer Institute, Bethesda, MD 20892-5055, USA.
Mi-Jin Kang
Adam M Suchar
Takeshi Shimamura
Ethan A Kohn
Aleksandra M Michalowska
V Craig Jordan
Setsuo Hirohashi
Lalage M Wakefield
National Cancer Institute · MYCenter for Biologics Evaluation and Research · USFox Chase Cancer Center · US

Funding

TGF-betas in breast cancer progressionZ01BC005785 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI WAKEFIELD, LALAGE · 1996 to 2008
$1.9M
Intramural NIH HHSNCI NIH HHS Z01 BC005785-11
6 · The paper itself

Abstract

Dysadherin, a cancer-associated membrane glycoprotein, down-regulates E-cadherin and promotes cancer metastasis. This study examined the role of dysadherin in breast cancer progression. Expression of dysadherin was found to be highest in breast cancer cell lines and tumors that lacked the estrogen receptor (ER). Knockdown of dysadherin caused increased association of E-cadherin with the actin cytoskeleton in breast cancer cell lines that expressed E-cadherin. However, knockdown of dysadherin could still suppress cell invasiveness in cells that had no functional E-cadherin, suggesting the existence of a novel mechanism of action. Global gene expression analysis identified chemokine (C-C motif) ligand 2 (CCL2) as the transcript most affected by dysadherin knockdown in MDA-MB-231 cells, and dysadherin was shown to regulate CCL2 expression in part through activation of the nuclear factor-kappaB pathway. The ability of dysadherin to promote tumor cell invasion in vitro was dependent on the establishment of a CCL2 autocrine loop, and CCL2 secreted by dysadherin-positive tumor cells also promoted endothelial cell migration in a paracrine fashion. Finally, experimental suppression of CCL2 in MDA-MB-231 cells reduced their ability to metastasize in vivo. This study shows that dysadherin has prometastatic effects that are independent of E-cadherin expression and that CCL2 could play an important role in mediating the prometastatic effect of dysadherin in ER-negative breast cancer.

Indexed as

ActinsBreast NeoplasmsCadherinsCell Line, TumorChemokine CCL2Endothelial CellsHumansIon ChannelsMembrane GlycoproteinsMicrofilament ProteinsNeoplasm MetastasisNeoplasm ProteinsNF-kappa BReceptors, EstrogenRNA, Small InterferingSignal TransductionActinsCadherinsCCL2 protein, humanChemokine CCL2FXYD5 protein, humanIon ChannelsMembrane GlycoproteinsMicrofilament ProteinsNeoplasm ProteinsNF-kappa BReceptors, EstrogenRNA, Small Interfering

Identifiers

PMID16849564
PMCPMC1557381
OpenAlexW2118566883

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.