Evidence map›Paper›PMID 41258756›Full record

ArticleAging cell2025

Senescent Fibroblasts Drive Melanoma Progression Through GCP-2 Induced CREB Phosphorylation Enhancing Glycolysis.

Abhijit Basu, Vida Farsam, Karmveer Singh, Diana Crisan, Nicolai Treiber, Lars Alexander Schneider, Margit Huber, Jennifer I Engelmeyer, Björn Schumacher, Pallab Maity and 6 more

Abstract read
In one paragraph

Article in Aging cell, 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

16 authors.

Abhijit BasuDepartment of Dermatology and Allergic Diseases, University of Ulm, Ulm, Germany.ORCID 0000-0002-7176-250X
Vida FarsamDepartment of Dermatology and Allergic Diseases, University of Ulm, Ulm, Germany.
Karmveer SinghDepartment of Dermatology and Allergic Diseases, University of Ulm, Ulm, Germany.ORCID 0000-0002-1237-7417
Diana CrisanDepartment of Dermatology and Allergic Diseases, University of Ulm, Ulm, Germany.ORCID 0000-0002-7479-5454
Nicolai TreiberDepartment of Dermatology and Allergic Diseases, University of Ulm, Ulm, Germany.ORCID 0009-0003-4530-0840
Lars Alexander SchneiderDepartment of Dermatology and Allergic Diseases, University of Ulm, Ulm, Germany.ORCID 0000-0001-8026-795X
Margit HuberDepartment of Dermatology and Allergic Diseases, University of Ulm, Ulm, Germany.
Jennifer I EngelmeyerInstitute for Genome Stability in Ageing and Disease, Medical Faculty and Cologne Excellence Cluster for Cellular Stress Responses in Ageing-Associated Diseases (CECAD) Research, University of Cologne, Cologne, Germany.ORCID 0009-0002-8831-0232
Björn SchumacherInstitute for Genome Stability in Ageing and Disease, Medical Faculty and Cologne Excellence Cluster for Cellular Stress Responses in Ageing-Associated Diseases (CECAD) Research, University of Cologne, Cologne, Germany.ORCID 0000-0001-6097-5238
Pallab MaityDepartment of Dermatology and Allergic Diseases, University of Ulm, Ulm, Germany.ORCID 0000-0001-9769-3533
Daniel BrandtHelmholtz Diabetes Center & German Diabetes Center (DZD), Helmholtz Zentrum München, Division of Metabolic Diseases, Technische Universität München, Neuherberg, Germany.ORCID 0000-0002-1589-3695
Martin JastrochHelmholtz Diabetes Center & German Diabetes Center (DZD), Helmholtz Zentrum München, Division of Metabolic Diseases, Technische Universität München, Neuherberg, Germany.ORCID 0000-0003-0358-3865
Cornelia MauchDepartment of Dermatology and Venereology, University of Cologne, Cologne, Germany.ORCID 0000-0002-3989-0536
Hartmut GeigerAging Research Center (ARC), University of Ulm, Ulm, Germany.ORCID 0000-0002-5794-5430
Dimitris KletsasLaboratory of Cell Proliferation & Ageing, Institute of Biosciences and Applications, NCSR "Demokritos", Athens, Greece.ORCID 0000-0002-9828-3963
Karin Scharffetter-KochanekDepartment of Dermatology and Allergic Diseases, University of Ulm, Ulm, Germany.ORCID 0000-0002-9655-685X

Funding

Bundesministerium für Bildung und Forschung 02NUK003BDeutsche Forschungsgemeinschaft KFO142; CRC1506
6 · The paper itself

Abstract

Aging constitutes the largest risk factor for melanoma progression. While a contribution of factors secreted from senescent skin fibroblasts to the progression of melanoma has been proposed, the nature of such factors and subsequent underlying mechanisms remains elusive. Here we show that the chemokine GCP-2 is excessively released by senescent fibroblasts in vitro and the skin of old melanoma patients. GCP-2 regulates, via phosphorylation of the transcription factor CREB at serine 133, defense-, cell cycle control-, and glycolysis-enhancing genes in melanoma cell lines. GCP-2 promotes oncogenic properties in vitro and in vivo in murine melanoma models. Inhibition of CREB phosphorylation in melanoma cells represses glycolytic target genes and induces a switch from glycolysis to oxidative phosphorylation that translates into a significant decline in tumor size in vivo in murine melanoma models. This study identifies a senescent fibroblast to chemokine to CREB to metabolic axis that drives melanoma progression. Targeting this axis may hold promise for novel therapeutic approaches in difficult-to-treat melanoma in older adults.

Indexed as

Cellular SenescenceCyclic AMP Response Element-Binding ProteinFibroblastsGlycolysisMelanomaSkin NeoplasmsAnimalsCell Line, TumorDisease ProgressionHumansMicePhosphorylationCyclic AMP Response Element-Binding ProteinCREBGCP‐2melanoma metabolismmelanoma progressionSASPsenescent fibroblast

Identifiers

PMID41258756
PMCPMC12686573

What OpenQuestion holds

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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.