Evidence map›Paper›PMID 21674054›Full record

ArticlePloS one2011

Transmigration of melanoma cells through the blood-brain barrier: role of endothelial tight junctions and melanoma-released serine proteases.

Csilla Fazakas, Imola Wilhelm, Péter Nagyoszi, Attila E Farkas, János Haskó, Judit Molnár, Hannelore Bauer, Hans-Christian Bauer, Ferhan Ayaydin, Ngo Thi Khue Dung and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed
7.3field-weighted citation impact, top 3% 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

84 citing papers in PubMed, 146 citations in OpenAlex.

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  13. Targeting of endothelial cells in brain tumours.Clinical and translational medicine · 2023
    Review
  14. The origin of brain malignancies at the blood-brain barrier.Cellular and molecular life sciences : CMLS · 2023
    Review
  15. Article
  16. Brain metastasis in breast cancer: focus on genes and signaling pathways involved, blood-brain barrier and treatment strategies.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Review
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24 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

12 authors at 3 institutions in 2 countries.

Csilla FazakasInstitute of Biophysics, Biological Research Center, Szeged, Hungary.
Imola Wilhelm
Péter Nagyoszi
Attila E Farkas
János Haskó
Judit Molnár
Hannelore Bauer
Hans-Christian Bauer
Ferhan Ayaydin
Ngo Thi Khue Dung
László Siklós
István A Krizbai
Institute of Biophysics · HUUniversity of Salzburg · ATHUN-REN Szegedi Biológiai Kutatóközpont · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Malignant melanoma represents the third common cause of brain metastasis, having the highest propensity to metastasize to the brain of all primary neoplasms in adults. Since the central nervous system lacks a lymphatic system, the only possibility for melanoma cells to reach the brain is via the blood stream and the blood-brain barrier. Despite the great clinical importance, mechanisms of transmigration of melanoma cells through the blood-brain barrier are incompletely understood. In order to investigate this question we have used an in vitro experimental setup based on the culture of cerebral endothelial cells (CECs) and the A2058 and B16/F10 melanoma cell lines, respectively. Melanoma cells were able to adhere to confluent brain endothelial cells, a process followed by elimination of protrusions and transmigration from the luminal to the basolateral side of the endothelial monolayers. The transmigration process of certain cells was accelerated when they were able to use the routes preformed by previously transmigrated melanoma cells. After migrating through the endothelial monolayer several melanoma cells continued their movement beneath the endothelial cell layer. Melanoma cells coming in contact with brain endothelial cells disrupted the tight and adherens junctions of CECs and used (at least partially) the paracellular transmigration pathway. During this process melanoma cells produced and released large amounts of proteolytic enzymes, mainly gelatinolytic serine proteases, including seprase. The serine protease inhibitor Pefabloc® was able to decrease to 44-55% the number of melanoma cells migrating through CECs. Our results suggest that release of serine proteases by melanoma cells and disintegration of the interendothelial junctional complex are main steps in the formation of brain metastases in malignant melanoma.

Indexed as

Transendothelial and Transepithelial MigrationAnimalsBlood-Brain BarrierCell Line, TumorEndothelial CellsHumansMelanomaMiceRatsSerine ProteasesTight JunctionsSerine Proteases

Identifiers

PMID21674054
PMCPMC3107231
OpenAlexW1985649889

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.