Evidence map›Paper›PMID 40645003›Full record

ArticleBiochemical and biophysical research communications2025

Aquaporin 5 transfer via MDA-MB-231 cell extracellular vesicles increases recipient endothelial cell invasion.

Ian M Smith, Allison K Moses, Ken D Brandon, Stephanie M Kronstadt, Autumn C Hengen, Emily H Powsner, Daniel H Levy, Sai Pranav Majeti Venkata, Nicholas H Pirolli, Steven M Jay and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Biochemical and biophysical research communications, 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. Review
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.

Ian M SmithFischell Department of Bioengineering, University of Maryland, College Park, MD, 20742, USA.
Allison K MosesFischell Department of Bioengineering, University of Maryland, College Park, MD, 20742, USA.
Ken D BrandonFischell Department of Bioengineering, University of Maryland, College Park, MD, 20742, USA.
Stephanie M KronstadtFischell Department of Bioengineering, University of Maryland, College Park, MD, 20742, USA.
Autumn C HengenFischell Department of Bioengineering, University of Maryland, College Park, MD, 20742, USA; Department of Bioengineering, Georgia Institute of Technology, Atlanta, GA, 30332, USA.
Emily H PowsnerFischell Department of Bioengineering, University of Maryland, College Park, MD, 20742, USA.
Daniel H LevyFischell Department of Bioengineering, University of Maryland, College Park, MD, 20742, USA.
Sai Pranav Majeti VenkataFischell Department of Bioengineering, University of Maryland, College Park, MD, 20742, USA.
Nicholas H PirolliFischell Department of Bioengineering, University of Maryland, College Park, MD, 20742, USA.
Steven M JayFischell Department of Bioengineering, University of Maryland, College Park, MD, 20742, USA; Fischell Institute for Biomedical Devices, University of Maryland, College Park, MD, 20742, USA; Program in Molecular and Cell Biology, University of Maryland, College Park, MD, 20742, USA; Marlene and Stewart Greenebaum Comprehensive Cancer Center, University of Maryland School of Medicine, Baltimore, MD, 21201, USA.
Kimberly M StrokaFischell Department of Bioengineering, University of Maryland, College Park, MD, 20742, USA; Marlene and Stewart Greenebaum Comprehensive Cancer Center, University of Maryland School of Medicine, Baltimore, MD, 21201, USA; Biophysics Program, University of Maryland, College Park, MD, 20742, USA; Center for Stem Cell Biology and Regenerative Medicine, University of Maryland, Baltimore, MD, 21201, USA. Electronic address: kstroka@umd.edu.

Funding

Exploring mechanisms of aquaporin-mediated cell migrationR35GM142838 · NIGMS · UNIV OF MARYLAND, COLLEGE PARK · PI STROKA, KIMBERLY · 2021 to 2025
$1.9M
NIGMS NIH HHS R35 GM142838
6 · The paper itself

Abstract

Aquaporin 5 (AQP5), a water channel protein, is a known promoter of cancer metastasis, primarily through its role in enhancing cancer cell motility and invasion. While this function has been studied extensively in cancer cells themselves, the contribution of AQP5 to the behavior of other cells in the tumor microenvironment, particularly endothelial cells, remains less understood. Prior studies have linked secreted signals from cancer cells with higher AQP5 expression to increased endothelial angiogenic capacity, a key driver of metastasis. Separately, metastasis-associated proteins have been shown to transfer from cancer to endothelial cells via extracellular vesicles (EVs), promoting angiogenesis. In this study, we investigated whether AQP5-containing EVs influence endothelial cell behavior. We found that EVs derived from cancer cells with high AQP5 expression significantly enhanced the invasive capacity of recipient endothelial cells, a process essential to angiogenesis. These findings provide the first evidence that transfer of the prometastatic protein AQP5 via EVs can modulate endothelial cell function, highlighting a novel mechanism by which cancer cells manipulate their microenvironment to support metastasis.

Indexed as

Aquaporin 5Breast NeoplasmsEndothelial CellsExtracellular VesiclesCell Line, TumorCell MovementFemaleHumansMDA-MB-231 CellsNeoplasm InvasivenessNeovascularization, PathologicTumor MicroenvironmentAQP5 protein, humanAquaporin 5Angiogenic invasionAquaporinCancer angiogenesisExosomesExtracellular vesicles

Identifiers

PMID40645003
PMCPMC12908701

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Registered trials

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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.