Evidence map›Paper›PMID 40435350›Full record

ArticlePloS one2025

The antiangiogenic peptide VIAN-c4551 inhibits lung melanoma metastasis in mice by reducing pulmonary vascular permeability.

Alma Lorena Perez, Magdalena Zamora, Manuel Bahena, Regina Aramburo-Williams, Elva Adan-Castro, Daniela Granados-Carrasco, Thomas Bertsch, Jakob Triebel, Gonzalo Martinez de la Escalera, Juan Pablo Robles and 1 more

Abstract read
In one paragraph

Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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

11 authors.

Alma Lorena PerezInstituto de Neurobiología, Universidad Nacional Autónoma de México (UNAM), Querétaro, México.
Magdalena ZamoraInstituto de Neurobiología, Universidad Nacional Autónoma de México (UNAM), Querétaro, México.
Manuel BahenaInstituto de Neurobiología, Universidad Nacional Autónoma de México (UNAM), Querétaro, México.
Regina Aramburo-WilliamsInstituto de Neurobiología, Universidad Nacional Autónoma de México (UNAM), Querétaro, México.
Elva Adan-CastroInstituto de Neurobiología, Universidad Nacional Autónoma de México (UNAM), Querétaro, México.
Daniela Granados-CarrascoInstituto de Neurobiología, Universidad Nacional Autónoma de México (UNAM), Querétaro, México.
Thomas BertschInstitute for Clinical Chemistry, Laboratory Medicine and Transfusion Medicine, Nuremberg General Hospital & Paracelsus Medical University, Nuremberg, Germany.
Jakob TriebelInstitute for Clinical Chemistry, Laboratory Medicine and Transfusion Medicine, Nuremberg General Hospital & Paracelsus Medical University, Nuremberg, Germany.ORCID 0000-0002-1989-8645
Gonzalo Martinez de la EscaleraInstituto de Neurobiología, Universidad Nacional Autónoma de México (UNAM), Querétaro, México.
Juan Pablo RoblesInstituto de Neurobiología, Universidad Nacional Autónoma de México (UNAM), Querétaro, México.
Carmen ClappInstituto de Neurobiología, Universidad Nacional Autónoma de México (UNAM), Querétaro, México.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionCancer cells drive the increase in vascular permeability mediating tumor cell extravasation and metastatic seeding. VIAN-c4551, an antiangiogenic peptide analog of vasoinhibin, inhibits the growth and vascularization of melanoma tumors in mice. Because VIAN-c4551 is a potent inhibitor of vascular permeability, we evaluated whether its antitumor action extended to a reduction in metastasis generation.

methodsCirculating levels of vascular endothelial growth factor (VEGF), lung vascular permeability, melanoma cell extravasation, and melanoma pulmonary nodules were assessed in C57BL/6J mice intravenously inoculated with murine melanoma B16-F10 cells after acute treatment with VIAN-c4551. VEGF levels, transendothelial electrical resistance, and transendothelial migration in cocultures of B16-F10 cells and endothelial cell monolayers supported the findings.

resultsB16-F10 cells increased circulating VEGF levels and elevated lung vascular permeability 2 hours after inoculation. VIAN-c4551 prevented enhanced vascular permeability and reduced melanoma cell extravasation after 2 hours and the number and size of macroscopic and microscopic melanoma tumors in lungs after 17 days. In vitro, VIAN-c4551 suppressed the B16-F10 cell-induced and VEGF mediated increase in endothelial cell monolayer permeability and the transendothelial migration of B16-F10 cells. No detrimental effect of VIAN-c4551 was observed on hematological, biochemical, and histological parameters after its intravenous administration in mice for 14 days.

conclusionsThese findings support the inhibition of distant vascular permeability for the prevention of tumor metastasis and unveil the anti-vascular permeability factor VIAN-c4551 as a potential and safe therapeutic drug able to prevent metastasis generation by lowering the extravasation of melanoma cells.

Indexed as

Angiogenesis InhibitorsCapillary PermeabilityLung NeoplasmsMelanoma, ExperimentalAnimalsCell Line, TumorHumansLungMiceMice, Inbred C57BLTransendothelial and Transepithelial MigrationVascular Endothelial Growth Factor AAngiogenesis InhibitorsVascular Endothelial Growth Factor A

Identifiers

PMID40435350
PMCPMC12118997

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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.