Evidence map›Paper›PMID 11498790›Full record

ArticleOncogene2001

Mel-CAM-specific genetic suppressor elements inhibit melanoma growth and invasion through loss of gap junctional communication.

K Satyamoorthy, J Muyrers, F Meier, D Patel, M Herlyn

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.9field-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

25 citing papers in PubMed, 76 citations in OpenAlex.

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  19. Cell signaling. Wnt moves beyond the canon.Science (New York, N.Y.) · 2008
    Article
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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

5 authors at 1 institution in 1 country.

K SatyamoorthyThe Wistar Institute, 3601 Spruce Street, Philadelphia, Pennsylvania, PA 19104 USA.
J Muyrers
F Meier
D Patel
M Herlyn
The Wistar Institute · US

Funding

Tumor Microenvironment and MetastasisP30CA010815 · NCI · WISTAR INSTITUTE · PI Luis J Montaner · 1985 to 2026
$75.9M
TRANSGENIC AND CHIMERIC MOUSE COREP30DK050306 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI Ken Hashigiwa Cadwell · 1997 to 2026
$32.5M
TUMOR DEVELOPMENT AND PROGRESSION IN HUMAN MELANOCYTESP01CA025874 · NCI · WISTAR INSTITUTE · PI HERLYN, MEENHARD F · 1985 to 2015
$19.0M
CELL/CELL COMMUNICATION DURING MELANOMA PROGRESSIONR01CA076674 · NCI · WISTAR INSTITUTE · PI HERLYN, MEENHARD F · 1998 to 2015
$4.0M
METASTATIS: BIOLOGICAL PHENOTYPE AND MODELS FOR THERAPYR01CA047159 · NCI · WISTAR INSTITUTE · PI HERLYN, MEENHARD F · 1989 to 2015
$3.9M
STRUCTURE/FUNCTION OF THE CO17-1A/GA733 ANTIGENP01CA074294 · NCI · WISTAR INSTITUTE · PI HERLYN, DOROTHEE M · 1998 to 2002
$3.9M
NCI NIH HHS CA10815NCI NIH HHS CA25874NCI NIH HHS CA47159NCI NIH HHS CA74294NCI NIH HHS CA76674NIDDK NIH HHS DK50306
6 · The paper itself

Abstract

Normal human melanocytes are interspersed singly among keratinocytes along the basement membrane of the epidermis, whereas melanoma cells readily adhere to each other during invasion of the dermis or distant organs. The tumorigenic and metastatic phenotype of melanoma cells often correlates with increased expression of cell-cell and cell-matrix adhesion receptors. Mel-CAM (MCAM, MUC 18, CD146) is a cell-cell adhesion receptor highly expressed by melanoma cells but not normal melanocytes. We show here that inhibition of Mel-CAM expression in metastatic melanoma cells using genetic suppressor elements of Mel-CAM cDNA leads to inhibition of adhesion between melanoma cells and to downregulation of the tumorigenic phenotype. Growth was not inhibited in genetic suppressor elements-transduced melanoma cells cultured in monolayers but was inhibited when cells were maintained anchorage-independently in soft agar and greatly reduced in immunodeficient mice. A three-dimensional epidermal skin equivalent model demonstrated that Mel-CAM allows melanoma cells to separate from the epidermis and invade the basement membrane zone and dermis. However, melanoma cells with little or no Mel-CAM were poorly invasive, possibly due to their loss of gap junctional communication. These results suggest the multifunctional role of a melanoma-associated cell-cell adhesion receptor in tumor progression.

Indexed as

Antigens, CDCell CommunicationGap JunctionsMembrane GlycoproteinsNeural Cell Adhesion MoleculesAnimalsAntigens, SurfaceApoptosisCD146 AntigenCell AdhesionCell DivisionCells, CulturedDNA, AntisenseDown-RegulationHumansMelanomaAntigens, CDAntigens, SurfaceCD146 AntigenDNA, AntisenseMCAM protein, humanMcam protein, mouseMembrane GlycoproteinsNeural Cell Adhesion Molecules

Identifiers

PMID11498790
OpenAlexW2329591400

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.