Evidence map›Paper›PMID 41009392›Full record

ArticleInternational journal of molecular sciences2025

A 'Spicy' Mechanotransduction Switch: Capsaicin-Activated TRPV1 Receptor Modulates Osteosarcoma Cell Behavior and Drug Sensitivity.

Arianna Buglione, David Becerril Rodriguez, Simone Dogali, Giulia Alloisio, Chiara Ciaccio, Marco Luce, Stefano Marini, Luisa Campagnolo, Antonio Cricenti, Magda Gioia

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In one paragraph

Article in International journal of molecular sciences, 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

10 authors.

Arianna BuglioneDepartment of Clinical Sciences and Translational Medicine, University of Rome Tor Vergata, 00133 Rome, Italy.ORCID 0009-0003-9729-1886
David Becerril RodriguezDepartment of Sciences, Roma Tre University, 00154 Rome, Italy.
Simone DogaliDepartment of Clinical Sciences and Translational Medicine, University of Rome Tor Vergata, 00133 Rome, Italy.ORCID 0009-0009-0294-5642
Giulia AlloisioDepartment of Clinical Sciences and Translational Medicine, University of Rome Tor Vergata, 00133 Rome, Italy.ORCID 0009-0008-3939-4752
Chiara CiaccioDepartment of Clinical Sciences and Translational Medicine, University of Rome Tor Vergata, 00133 Rome, Italy.ORCID 0000-0003-1119-2303
Marco LuceInstitute of Structure Matter del Consiglio Nazionale delle Ricerche ISM-CNR, 00133 Rome, Italy.
Stefano MariniDepartment of Clinical Sciences and Translational Medicine, University of Rome Tor Vergata, 00133 Rome, Italy.
Luisa CampagnoloDepartment of Biomedicine and Prevention, University of Rome Tor Vergata, 00133 Rome, Italy.ORCID 0000-0003-3928-0276
Antonio CricentiInstitute of Structure Matter del Consiglio Nazionale delle Ricerche ISM-CNR, 00133 Rome, Italy.ORCID 0000-0002-8581-3478
Magda GioiaDepartment of Clinical Sciences and Translational Medicine, University of Rome Tor Vergata, 00133 Rome, Italy.ORCID 0000-0003-0352-3547

Funding

Italian Ministry of University and Research (MUR) 6992022PFFPBLTor Vergata" University of Rome UBP_GioiaM_CAMA-Gioia RSA TIPO B
6 · The paper itself

Abstract

Osteosarcoma (OS), the most common primary malignant bone tumor, arises in highly mechanosensitive tissue and exhibits marked heterogeneity and resistance to conventional therapies. While molecular drivers have been extensively characterized, the role of mechanical stimuli in OS progression remains underexplored. Here, we identify the transient receptor potential vanilloid 1 (TRPV1) channel as a key regulator of mechanotransduction and drug responsiveness in OS cells. Using uniaxial cyclic stretch, we show that aggressive U-2 OS cells undergo TRPV1-dependent perpendicular reorientation, unlike the inert SAOS-2 cells. Confocal microscopy, immunohistochemistry, and atomic force microscopy reveal that nanomolar concentrations of capsaicin-a well-characterized TRPV1 agonist-chemically mimic this mechanical phenotype, altering metastatic traits including adhesion, edge architecture, migration, nuclear-to-cytoplasmic ratio, and sensitivity to doxorubicin and cisplatin. TRPV1 activation, whether mechanical or chemical, induces subtype-specific effects absent in healthy hFOB osteoblasts. Notably, it differentially regulates nuclear localization of the proto-oncogene Src in U-2 OS versus SAOS-2 cells. Corresponding changes in Src and acetylated histone H3 (acH3) levels support a role for TRPV1 in modulating the Src-acH3 mechanosignaling axis. These effects are tumor-specific, positioning TRPV1 as a mechanosensitive signaling hub that integrates mechanical and chemical cues to drive epigenetic remodeling and phenotypic plasticity in OS, with potential as a therapeutic target in aggressive, drug-resistant subtypes.

Indexed as

Bone NeoplasmsCapsaicinDrug Resistance, NeoplasmMechanotransduction, CellularOsteosarcomaTRPV Cation ChannelsAntineoplastic AgentsCell Line, TumorCell MovementCisplatinDoxorubicinHistonesHumansProto-Oncogene MasAntineoplastic AgentsCapsaicinCisplatinDoxorubicinHistonesMAS1 protein, humanProto-Oncogene MasTRPV1 protein, humanTRPV Cation Channelscapsaicincell adhesioncell reorientationcyclic stretchhistone H3 acetylationmechanosensitive ion channelsmechanotransductionosteosarcomaSrc kinaseTRPV1

Identifiers

PMID41009392
PMCPMC12469300

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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.