Evidence map›Paper›PMID 40386826›Full record

ArticleCancer medicine2025

NSD2 and miRNAs as Key Regulators of Melanoma Response to Romidepsin and Interferon-α2b Treatment.

Alessandro De Santis, Lucrezia De Santis, Francesca Rossi, Silvia Gasparini, Valerio Licursi, Vito Antonio Amico, Imerio Capone, Alessandra Fragale, Stefania D'atri, Lucia Gabriele and 1 more

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In one paragraph

Article in Cancer medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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.

Alessandro De SantisDepartment of Biology and Biotechnology Charles Darwin, Sapienza University of Rome, Rome, Italy.
Lucrezia De SantisDepartment of Biology and Biotechnology Charles Darwin, Sapienza University of Rome, Rome, Italy.
Francesca RossiMax Planck Institute for Molecular Genetics, Chromatin Structure and Function, Berlin, Germany.ORCID https://orcid.org/0000-0002-1696-7078
Silvia GaspariniInstitute of Molecular Biology and Pathology (IBPM), National Research Council (CNR) of Italy, Rome, Italy.
Valerio LicursiInstitute of Molecular Biology and Pathology (IBPM), National Research Council (CNR) of Italy, Rome, Italy.
Vito Antonio AmicoDepartment of Biology and Biotechnology Charles Darwin, Sapienza University of Rome, Rome, Italy.
Imerio CaponeMolecular Oncology Laboratory, Istituto Dermatopatico Dell'immacolata IDI-IRCCS, Rome, Italy.
Alessandra FragaleMolecular Oncology Laboratory, Istituto Dermatopatico Dell'immacolata IDI-IRCCS, Rome, Italy.
Stefania D'atriMolecular Oncology Laboratory, Istituto Dermatopatico Dell'immacolata IDI-IRCCS, Rome, Italy.
Lucia GabrieleMolecular Oncology Laboratory, Istituto Dermatopatico Dell'immacolata IDI-IRCCS, Rome, Italy.
Carlo PresuttiDepartment of Biology and Biotechnology Charles Darwin, Sapienza University of Rome, Rome, Italy.ORCID https://orcid.org/0000-0003-3837-2275

Funding

University of Rome La Sapienza PNRR CN3 - RNA_Spoke3
6 · The paper itself

Abstract

backgroundWe investigated the role of Nuclear Receptor Binding SET Domain Protein 2 (NSD2) and microRNAs (miRNAs) in melanoma de-differentiation following Romidepsin and Interferon-α2b (RI) treatment. Melanoma is the most lethal form of skin cancer, and despite advancements in therapy, treatment resistance remains a major challenge. De-differentiation has been widely recognized as a key factor contributing to therapy resistance.

methodsRNA-seq and TCGA transcriptomic data were re-analyzed to identify miRNAs and NSD2 expressions. The functional impact of selected miRNAs was then investigated at the molecular and phenotypic levels using primary and immortalized cell lines.

resultsOur findings demonstrate that RI treatment induces a de-differentiation process in primary melanoma cells, resembling that observed in therapy-resistant melanoma. This effect is particularly pronounced in cells with an intrinsic proliferative phenotype, where we observed significant downregulation of NSD2, a key epigenetic regulator implicated in multiple cancers. Additionally, we identified specific miRNAs as mediators of NSD2 downregulation, influencing melanoma cell viability and fitness.

conclusionsThese findings provide new insights into the molecular mechanisms driving melanoma progression and highlight potential therapeutic targets to counteract treatment resistance.

Indexed as

DepsipeptidesHistone-Lysine N-MethyltransferaseMelanomaMicroRNAsSkin NeoplasmsCell Line, TumorCell ProliferationDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHumansInterferon alpha-2DepsipeptidesHistone-Lysine N-MethyltransferaseInterferon alpha-2MicroRNAsromidepsinepigenetic regulationmelanomamicroRNAsNSD2proliferative subtypes

Identifiers

PMID40386826
PMCPMC12086509

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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.