Evidence map›Paper›PMID 38310103›Full record

ArticleNature communications2024

ANKRD1 is a mesenchymal-specific driver of cancer-associated fibroblast activation bridging androgen receptor loss to AP-1 activation.

Luigi Mazzeo, Soumitra Ghosh, Emery Di Cicco, Jovan Isma, Daniele Tavernari, Anastasia Samarkina, Paola Ostano, Markus K Youssef, Christian Simon, G Paolo Dotto

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
9.6field-weighted citation impact, top 1% of its field
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

30 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025
    Article
  18. Review
  19. Article
  20. 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

10 authors at 6 institutions in 3 countries.

Luigi MazzeoDepartment of Immunobiology, University of Lausanne, Epalinges, Switzerland.
Soumitra GhoshORL service, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland.
Emery Di CiccoCutaneous Biology Research Center, Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
Jovan IsmaDepartment of Immunobiology, University of Lausanne, Epalinges, Switzerland.
Daniele TavernariDepartment of Computational Biology, University of Lausanne, Lausanne, Switzerland.ORCID 0000-0001-5981-7363
Anastasia SamarkinaDepartment of Immunobiology, University of Lausanne, Epalinges, Switzerland.ORCID 0000-0003-1553-4366
Paola OstanoCancer Genomics Laboratory, Edo and Elvo Tempia Valenta Foundation, Biella, 13900, Italy.ORCID 0000-0002-4000-2954
Markus K YoussefDepartment of Immunobiology, University of Lausanne, Epalinges, Switzerland.ORCID 0000-0002-5754-1938
Christian SimonORL service, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland.
G Paolo DottoDepartment of Immunobiology, University of Lausanne, Epalinges, Switzerland. gdotto@mgh.harvard.edu.ORCID 0000-0002-1197-8448
University of Lausanne · CHHarvard University · USUniversity Hospital of Lausanne · CHFondazione Edo ed Elvo Tempia · ITPrevention Institute · USSIB Swiss Institute of Bioinformatics · CH

Funding

GROWTH DIFFERENTIATION CONTROL IN PRIMARY KERATINOCYTES.R01AR039190 · NIAMS · YALE UNIVERSITY · PI DOTTO, GIAN-PAOLO · 1988 to 2021
$9.5M
Epigenetic control of skin homeostasis by the ULK3 nuclear kinaseR01AR078374 · NIAMS · MASSACHUSETTS GENERAL HOSPITAL · PI DOTTO, GIAN-PAOLO · 2021 to 2025
$2.4M
NIAMS NIH HHS R01 AR039190NIAMS NIH HHS R01 AR078374
6 · The paper itself

Abstract

There are significant commonalities among several pathologies involving fibroblasts, ranging from auto-immune diseases to fibrosis and cancer. Early steps in cancer development and progression are closely linked to fibroblast senescence and transformation into tumor-promoting cancer-associated fibroblasts (CAFs), suppressed by the androgen receptor (AR). Here, we identify ANKRD1 as a mesenchymal-specific transcriptional coregulator under direct AR negative control in human dermal fibroblasts (HDFs) and a key driver of CAF conversion, independent of cellular senescence. ANKRD1 expression in CAFs is associated with poor survival in HNSCC, lung, and cervical SCC patients, and controls a specific gene expression program of myofibroblast CAFs (my-CAFs). ANKRD1 binds to the regulatory region of my-CAF effector genes in concert with AP-1 transcription factors, and promotes c-JUN and FOS association. Targeting ANKRD1 disrupts AP-1 complex formation, reverses CAF activation, and blocks the pro-tumorigenic properties of CAFs in an orthotopic skin cancer model. ANKRD1 thus represents a target for fibroblast-directed therapy in cancer and potentially beyond.

Indexed as

Cancer-Associated FibroblastsSkin NeoplasmsFibroblastsHumansMuscle ProteinsNuclear ProteinsProto-Oncogene Proteins c-junReceptors, AndrogenRepressor ProteinsTranscription Factor AP-1Tumor MicroenvironmentANKRD1 protein, humanAR protein, humanJUN protein, humanMuscle ProteinsNuclear ProteinsProto-Oncogene Proteins c-junReceptors, AndrogenRepressor ProteinsTranscription Factor AP-1

Identifiers

PMID38310103
PMCPMC10838290
OpenAlexW4391509828

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.