Evidence map›Paper›PMID 39933141›Full record

ArticleThe Journal of clinical investigation2025

Integrative analysis reveals therapeutic potential of pyrvinium pamoate in Merkel cell carcinoma.

Jiawen Yang, James T Lim, Paul Victor Santiago Raj, Marcelo G Corona, Chen Chen, Hunain Khawaja, Qiong Pan, Gillian D Paine-Murrieta, Rick G Schnellmann, Denise J Roe and 3 more

Abstract read
In one paragraph

Article in The Journal of clinical investigation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors.

Jiawen YangUniversity of Arizona Cancer Center, Tucson, Arizona, USA.
James T LimDepartment of Molecular and Cellular Biology, University of Arizona, Tucson, Arizona, USA.
Paul Victor Santiago RajDepartment of Pharmacology and Toxicology, The University of Arizona R. Ken Coit College of Pharmacy, Skaggs Pharmaceutical Sciences Center, Tucson, Arizona, USA.
Marcelo G CoronaUniversity of Arizona Cancer Center, Tucson, Arizona, USA.
Chen ChenUniversity of Arizona Cancer Center, Tucson, Arizona, USA.
Hunain KhawajaUniversity of Arizona Cancer Center, Tucson, Arizona, USA.
Qiong PanDepartment of Molecular and Cellular Biology, University of Arizona, Tucson, Arizona, USA.
Gillian D Paine-MurrietaUniversity of Arizona Cancer Center, Tucson, Arizona, USA.
Rick G SchnellmannDepartment of Pharmacology and Toxicology, The University of Arizona R. Ken Coit College of Pharmacy, Skaggs Pharmaceutical Sciences Center, Tucson, Arizona, USA.
Denise J RoeDepartment of Epidemiology and Biostatistics, University of Arizona Mel and Enid Zuckerman College of Public Health, Tucson, AZ, USA.
Prafulla C GokhaleDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA.
James A DeCaprioDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA.
Megha PadiUniversity of Arizona Cancer Center, Tucson, Arizona, USA.

Funding

VITAMIN AP30CA023074 · NCI · UNIVERSITY OF ARIZONA · PI Dan Theodorescu · 1985 to 2026
$110.2M
The DREAM B-Myb-MuvB complex controls sensitivity to DNA replication activators and inhibitorsR35CA232128 · NCI · DANA-FARBER CANCER INST · PI DECAPRIO, JAMES A. · 2019 to 2025
$7.2M
Unraveling the regulatory circuits that drive Merkel cell carcinomaR01CA251729 · NCI · UNIVERSITY OF ARIZONA · PI PADI, MEGHA · 2021 to 2025
$1.7M
NCI NIH HHS P30 CA023074NCI NIH HHS R01 CA251729NCI NIH HHS R35 CA232128
6 · The paper itself

Abstract

Merkel Cell Carcinoma (MCC) is an aggressive neuroendocrine cutaneous malignancy arising from either ultraviolet-induced mutagenesis or Merkel cell polyomavirus (MCPyV) integration. Despite extensive research, our understanding of the molecular mechanisms driving the transition from normal cells to MCC remains limited. To address this knowledge gap, we assessed the impact of inducible MCPyV T antigens on normal human fibroblasts by performing RNA-seq. Our data uncovered changes in expression and regulation of Wnt signaling pathway members. Building on this observation, we bioinformatically evaluated various Wnt pathway perturbagens for their ability to reverse the MCC gene expression signature and identified pyrvinium pamoate, an FDA-approved anthelminthic drug known for its antitumor activity in other cancers. Leveraging transcriptomic, network, and molecular analyses, we found that pyrvinium targets multiple MCC vulnerabilities. Pyrvinium not only reverses the neuroendocrine features of MCC by modulating canonical and noncanonical Wnt signaling but also inhibits cancer cell growth by activating p53-mediated apoptosis, disrupting mitochondrial function, and inducing endoplasmic reticulum stress. Finally, we demonstrated that pyrvinium reduces tumor growth in an MCC mouse xenograft model. These findings offer a deeper understanding of the role of Wnt signaling in MCC and highlight the utility of pyrvinium as a potential treatment for MCC.

Indexed as

Carcinoma, Merkel CellPyrvinium CompoundsSkin NeoplasmsWnt Signaling PathwayAnimalsApoptosisCell Line, TumorHumansMerkel cell polyomavirusMiceXenograft Model Antitumor AssayspyrviniumPyrvinium CompoundsBioinformaticsDermatologyDrug therapyOncologySkin cancerVirology

Identifiers

PMID39933141
PMCPMC11957690

What OpenQuestion holds

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LicenceCC BY
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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.