Evidence map›Paper›PMID 40855049›Full record

ArticleNature communications2025

The HDAC inhibitor romidepsin renders liver cancer vulnerable to RTK targeting and immunologically active.

Celia Sequera, Margherita Grattarola, Floriane Cannet, Aurélie Dobric, Paula Michea Veloso, Melissa Methia, Sylvie Richelme, Abdessamad El Kaoutari, Paraskevi Kousteridou, Delphine Debayle and 15 more

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Review
  2. Article
  3. Crosstalk BetweenCancers · 2026
    Review
  4. Fimepinostat Promotes Apoptosis and Decreases Cytokine Secretion inInternational journal of molecular sciences · 2026
    Article
  5. Review
  6. 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

25 authors.

Celia Sequera *Aix Marseille Univ, CNRS, Inserm, Institut Paoli-Calmettes, Centre de Recherche en Cancérologie de Marseille (CRCM), Marseille, France. celia.SEQUERA-HURTADO@univ-amu.fr.ORCID http://orcid.org/0000-0001-6409-3910
Margherita Grattarola *Aix Marseille Univ, CNRS, Inserm, Institut Paoli-Calmettes, Centre de Recherche en Cancérologie de Marseille (CRCM), Marseille, France.
Floriane CannetAix Marseille Univ, CNRS, Inserm, Institut Paoli-Calmettes, Centre de Recherche en Cancérologie de Marseille (CRCM), Marseille, France.
Aurélie DobricAix Marseille Univ, CNRS, Inserm, Institut Paoli-Calmettes, Centre de Recherche en Cancérologie de Marseille (CRCM), Marseille, France.
Paula Michea VelosoAix Marseille Univ, CNRS, Inserm, Institut Paoli-Calmettes, Centre de Recherche en Cancérologie de Marseille (CRCM), Marseille, France.
Melissa MethiaAix Marseille Univ, CNRS, Inserm, Institut Paoli-Calmettes, Centre de Recherche en Cancérologie de Marseille (CRCM), Marseille, France.
Sylvie RichelmeAix Marseille Univ, CNRS, Developmental Biology Institute of Marseille (IBDM), Turing Center for Living Systems, Marseille, France.
Abdessamad El KaoutariAix Marseille Univ, CNRS, Inserm, Institut Paoli-Calmettes, Centre de Recherche en Cancérologie de Marseille (CRCM), Marseille, France.
Paraskevi KousteridouAix Marseille Univ, CNRS, Inserm, Institut Paoli-Calmettes, Centre de Recherche en Cancérologie de Marseille (CRCM), Marseille, France.
Delphine DebayleIPMC-CNRS, Plateforme d'analyse des biomolécules PAB-Azur, Valbonne, France.ORCID http://orcid.org/0000-0003-2807-9198
Lukas KüblerDepartment of Biomedicine, University Hospital Basel, University of Basel, Basel, Switzerland.
Sandro NuciforoDepartment of Biomedicine, University Hospital Basel, University of Basel, Basel, Switzerland.ORCID http://orcid.org/0000-0002-1863-1869
Yannick BoursierAix Marseille Univ, CNRS/IN2P3, CPPM, Marseille, France.
Mathieu DupontAix Marseille Univ, CNRS/IN2P3, CPPM, Marseille, France.
Stefania PizzimentiDepartment of Clinical and Biological Sciences, University of Turin, Turin, Italy.
Giuseppina BarreraDepartment of Clinical and Biological Sciences, University of Turin, Turin, Italy.
Jean-William DupuyUniv. Bordeaux, Plateforme Protéome, Bordeaux, France.ORCID http://orcid.org/0000-0002-2448-4797
Frédéric SaltelBordeaux University, Inserm, Oncoprot, UMS 005, UMR1312, BRIC, BoRdeaux Institute in onCology, Bordeaux, France.ORCID http://orcid.org/0000-0002-0724-9680
Markus H HeimDepartment of Biomedicine, University Hospital Basel, University of Basel, Basel, Switzerland.ORCID http://orcid.org/0000-0002-7523-4894
Sophie VasseurAix Marseille Univ, CNRS, Inserm, Institut Paoli-Calmettes, Centre de Recherche en Cancérologie de Marseille (CRCM), Marseille, France.ORCID http://orcid.org/0000-0002-2339-8854
Xavier AdhouteDepartment of Gastroenterology and Hepatology, Hôpital Saint-Joseph, Marseille, France.
Fabienne GuillaumondAix Marseille Univ, CNRS, Inserm, Institut Paoli-Calmettes, Centre de Recherche en Cancérologie de Marseille (CRCM), Marseille, France.ORCID http://orcid.org/0000-0001-7456-7315
Jean-Paul BorgAix Marseille Univ, CNRS, Inserm, Institut Paoli-Calmettes, Centre de Recherche en Cancérologie de Marseille (CRCM), Marseille, France.ORCID http://orcid.org/0000-0001-8418-3382
Christian MorelAix Marseille Univ, CNRS/IN2P3, CPPM, Marseille, France.ORCID http://orcid.org/0000-0001-5359-6504
Flavio MainaAix Marseille Univ, CNRS, Inserm, Institut Paoli-Calmettes, Centre de Recherche en Cancérologie de Marseille (CRCM), Marseille, France. flavio.maina@univ-amu.fr.ORCID http://orcid.org/0000-0001-6100-4695

Funding

Fondation de France 2016_00067080Institut National Du Cancer (French National Cancer Institute) 2020-11/279/NI-KA
6 · The paper itself

Abstract

Histone deacetylases (HDACs) are epigenetic regulators frequently altered in cancer. Here we report that overexpression of HDAC1/2 occurs in Hepatocellular Carcinoma (HCC) patients, correlating with poor prognosis. We show that romidepsin, a class-I HDAC inhibitor, elicits a combinatorial perturbation of distinct molecular processes in HCC cells, altering lipid composition, mitotic spindle machinery, and levels of cell cycle/survival signals. Collectively, these alterations lead HCC cells to a vulnerable state, conferring dependency to receptor tyrosine kinase (RTK) signalling support. The cytostatic effects of romidepsin alone is converted into cytotoxicity by the RTK inhibitor cabozantinib in HCC models. We document that romidepsin+cabozantibib confers an immune-stimulatory profile in Alb-R26

Indexed as

Carcinoma, HepatocellularDepsipeptidesHistone Deacetylase InhibitorsLiver NeoplasmsAnilidesAnimalsCell Line, TumorEpigenesis, GeneticFemaleHistone Deacetylase 1Histone Deacetylase 2HumansMaleMiceProtein Kinase InhibitorsPyridinesAnilidescabozantinibDepsipeptidesHDAC1 protein, humanHDAC2 protein, humanHistone Deacetylase 1Histone Deacetylase 2Histone Deacetylase InhibitorsProtein Kinase InhibitorsPyridinesromidepsin

Identifiers

PMID40855049
PMCPMC12378214

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.