Evidence map›Paper›PMID 41781748›Full record

ArticleCommunications biology2026

Intracellular complement Factor H promotes tumor progression through modulation of cell cycle and actin cytoskeleton.

Mikel Rezola Artero, Andrea Minery, Margot Revel, Angela Armento, Mohamed-Ali Jarboui, Idris Boudhabhay, Marina de Castro Deus, Alessandra Zarantonello, Emma Fleury, Lou Segarra and 9 more

Abstract read
In one paragraph

Article in Communications biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. 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

19 authors.

Mikel Rezola ArteroCentre de Recherche des Cordeliers, Inflammation, Complement and Cancer team, Sorbonne Université, Inserm, Université Paris Cité, Paris, France.
Andrea MineryCentre de Recherche des Cordeliers, Inflammation, Complement and Cancer team, Sorbonne Université, Inserm, Université Paris Cité, Paris, France.
Margot RevelCentre de Recherche des Cordeliers, Inflammation, Complement and Cancer team, Sorbonne Université, Inserm, Université Paris Cité, Paris, France.
Angela ArmentoDepartment for Ophthalmology, Institute for Ophthalmic Research, Eberhard Karls University of Tübingen, Tübingen, Germany.
Mohamed-Ali JarbouiDepartment for Ophthalmology, Institute for Ophthalmic Research, Eberhard Karls University of Tübingen, Tübingen, Germany.ORCID http://orcid.org/0000-0002-5203-235X
Idris BoudhabhayCentre de Recherche des Cordeliers, Inflammation, Complement and Cancer team, Sorbonne Université, Inserm, Université Paris Cité, Paris, France.ORCID http://orcid.org/0000-0002-8045-1658
Marina de Castro DeusCentre de Recherche des Cordeliers, Inflammation, Complement and Cancer team, Sorbonne Université, Inserm, Université Paris Cité, Paris, France.
Alessandra ZarantonelloCentre de Recherche des Cordeliers, Inflammation, Complement and Cancer team, Sorbonne Université, Inserm, Université Paris Cité, Paris, France.ORCID http://orcid.org/0000-0002-9769-2271
Emma FleuryCentre de Recherche des Cordeliers, Inflammation, Complement and Cancer team, Sorbonne Université, Inserm, Université Paris Cité, Paris, France.
Lou SegarraCentre de Recherche des Cordeliers, Inflammation, Complement and Cancer team, Sorbonne Université, Inserm, Université Paris Cité, Paris, France.
Alaeddine RedissiCentre de Recherche des Cordeliers, Inflammation, Complement and Cancer team, Sorbonne Université, Inserm, Université Paris Cité, Paris, France.
Nicolas S MerleCentre de Recherche des Cordeliers, Inflammation, Complement and Cancer team, Sorbonne Université, Inserm, Université Paris Cité, Paris, France.
Marie-Agnes Dragon-DureyCentre de Recherche des Cordeliers, Inflammation, Complement and Cancer team, Sorbonne Université, Inserm, Université Paris Cité, Paris, France.ORCID http://orcid.org/0000-0002-5809-8122
Catherine MonnotCentre de Recherche des Cordeliers, Inflammation, Complement and Cancer team, Sorbonne Université, Inserm, Université Paris Cité, Paris, France.ORCID http://orcid.org/0000-0003-1334-7348
Catherine Sautes-FridmanCentre de Recherche des Cordeliers, Inflammation, Complement and Cancer team, Sorbonne Université, Inserm, Université Paris Cité, Paris, France.ORCID http://orcid.org/0000-0003-1735-8722
Jordan D DimitrovCentre de Recherche des Cordeliers, Inflammation, Immunopathology and therapeutic immuno-intervention, Sorbonne Université, Inserm, Université Paris Cité, Paris, France.ORCID http://orcid.org/0000-0001-8536-8995
Wolf Herman FridmanCentre de Recherche des Cordeliers, Inflammation, Complement and Cancer team, Sorbonne Université, Inserm, Université Paris Cité, Paris, France.ORCID http://orcid.org/0000-0002-1332-0973
Marius UeffingDepartment for Ophthalmology, Institute for Ophthalmic Research, Eberhard Karls University of Tübingen, Tübingen, Germany.ORCID http://orcid.org/0000-0003-2209-2113
Lubka T RoumeninaCentre de Recherche des Cordeliers, Inflammation, Complement and Cancer team, Sorbonne Université, Inserm, Université Paris Cité, Paris, France. lubka.roumenina@inserm.fr.ORCID http://orcid.org/0000-0002-9940-0324

Funding

Fondation ARC pour la Recherche sur le Cancer (ARC Foundation for Cancer Research) ARCPJA2023080006999
6 · The paper itself

Abstract

Overexpression of complement genes in the tumor microenvironment, including Factor H (FH), is a strong predictor of poor prognosis in multiple cancers. Its canonical functions in the bloodborne complement cascade, though, cannot explain this prognostic impact. Here, we demonstrate that FH operates within the intracellular space in fibroblasts and tumor cells. By transcriptomics approach in patient tumors, cellular and biochemical assays we revealed that the prognostic impact of FH overexpression is mediated mainly by its cell-intrinsic functions in tumor-promoting fibroblasts and malignant cells. Intranuclear FH interacts with the cell cycle-transcription factor E2F3. FH also promotes proliferation by lowering the nuclear p53 pool. Moreover, in ccRCC cancer cells, FH also regulates cytoskeleton organization and cell morphology, potentially, via interaction with the actin capping CapZ complex. Therefore, complement FH acts as a multitasking effector, regulating cell cycle and actin polymerization, challenging the paradigm of extracellular space-restricted functioning, considered for many complement proteins.

Indexed as

Actin CytoskeletonCell CycleComplement Factor HAnimalsCell Line, TumorCell ProliferationDisease ProgressionGene Expression Regulation, NeoplasticHumansTumor MicroenvironmentComplement Factor H

Identifiers

PMID41781748
PMCPMC13076602

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.