Evidence map›Paper›PMID 41007281›Full record

ArticleBiology2025

Hypoxia-Driven Extracellular Vesicles Promote Pro-Metastatic Signalling in LNCaP Cells via Wnt and EMT Pathways.

Melissa Santos, Khansa Bukhari, Irem Peker-Eyüboğlu, Igor Kraev, Dafydd Alwyn Dart, Sigrun Lange, Pinar Uysal-Onganer

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Biology, 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

7 authors.

Melissa SantosCancer Mechanisms and Biomarkers Research Group, School of Life Sciences, University of Westminster, London W1W 6UW, UK.ORCID 0009-0002-4757-176X
Khansa BukhariCancer Mechanisms and Biomarkers Research Group, School of Life Sciences, University of Westminster, London W1W 6UW, UK.
Irem Peker-EyüboğluCancer Mechanisms and Biomarkers Research Group, School of Life Sciences, University of Westminster, London W1W 6UW, UK.
Igor KraevElectron Microscopy Suite, Faculty of Science, Technology, Engineering and Mathematics, Open University, Milton Keynes MK7 6AA, UK.ORCID 0000-0003-1822-278X
Dafydd Alwyn DartUCL Cancer Institute, University College London, Paul O'Gorman Building, 72 Huntley Street, London WC1E 6DD, UK.ORCID 0000-0003-3801-8583
Sigrun LangePathobiology and Extracellular Vesicles Research Group, School of Life Sciences, University of Westminster, London W1W 6UW, UK.ORCID 0000-0002-7193-3102
Pinar Uysal-OnganerCancer Mechanisms and Biomarkers Research Group, School of Life Sciences, University of Westminster, London W1W 6UW, UK.ORCID 0000-0003-3190-8831

Funding

The Quintin Hogg Trust, and Quality Related (QR) research funding to P U-O. and S.L. from the University of Westminster M.S., S.L and PU-O
6 · The paper itself

Abstract

Prostate cancer (PCa) progression is shaped by the tumour microenvironment, where hypoxia promotes aggressiveness and contributes to therapy resistance. Extracellular vesicles (EVs), secreted under hypoxia, can deliver modified bioactive cargo that reprograms recipient cells. This study examined whether EVs from hypoxia-conditioned metastatic PCa cells enhance malignant traits in cancerous and non-tumorigenic prostate cell lines via Wnt signalling and epithelial-mesenchymal transition (EMT). EVs from PC3 cells cultured under hypoxia (1% O

Indexed as

epithelial–mesenchymal transition (EMT)extracellular vesicles (EVs)HIF-1αhypoxiainvasionprostate cancertumour microenvironmentWnt signalling (Wnt)

Identifiers

PMID41007281
PMCPMC12467610

What Socratic 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 Socratic graph.