Evidence map›Paper›PMID 40229245›Full record

ReviewCell death & disease2025

Inflammation and cancer cell survival: TRAF2 as a key player.

Adriana Albini, Luisa Di Paola, Giampiero Mei, Denisa Baci, Nicola Fusco, Giovanni Corso, Douglas Noonan

Abstract readReview
In one paragraph

Review in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed.

  1. Article
  2. Decoding TNF receptor superfamily control of CD4Cell communication and signaling : CCS · 2026
    Review
  3. Article
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  6. Article
  7. Review
  8. Article
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  12. Article
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  19. Glycyrrhiza polysaccharide attenuatesFrontiers in veterinary science · 2025
    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

7 authors.

Adriana Albini *European Institute of Oncology (IEO), Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Milan, Italy. adriana.albini@ieo.it.ORCID http://orcid.org/0000-0002-9624-5103
Luisa Di Paola *Unit of Chemical-Physics Fundamentals in Chemical Engineering, Faculty Department of Science and Technology for Sustainable Development and One Health, Università Campus Bio-Medico, Rome, Italy.
Giampiero Mei *Department of Experimental Medicine, University of Rome Tor Vergata, Rome, Italy.
Denisa BaciDepartment of Biotechnology and Life Sciences, University of Insubria, Varese, Italy.
Nicola FuscoEuropean Institute of Oncology (IEO), Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Milan, Italy.
Giovanni CorsoDepartment of Oncology and Hemato-Oncology, University of Milan, Milan, Italy. giovanni.corso@ieo.it.
Douglas NoonanDepartment of Biotechnology and Life Sciences, University of Insubria, Varese, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TNF receptor-associated factor 2 (TRAF2) plays a crucial role in both physiological and pathological processes. It takes part in the regulation of cell survival and death, tissue regeneration, development, endoplasmic reticulum stress response, autophagy, homeostasis of the epithelial barrier and regulation of adaptive and innate immunity. Initially identified for its interaction with TNF receptor 2 (TNFR2), TRAF2 contains a TRAF domain that enables homo- and hetero-oligomerization, allowing it to interact with multiple receptors and signaling molecules. While best known for mediating TNFR1 and TNFR2 signaling, TRAF2 also modulates other receptor pathways, including MAPK, NF-κB, and Wnt/β-catenin cascades. By regulating NF-κB-inducing kinase (NIK), TRAF2 is a key activator of the alternative NF-κB pathway, linking it to inflammatory diseases, immune dysfunction, and tumorigenesis. In the innate immune system, TRAF2 influences macrophage differentiation, activation, and survival and stimulates natural killer cell cytotoxicity. In the adaptive immune system, it represses effector B- and T-cell activity while sustaining regulatory T-cell function, thus promoting immune suppression. The lack of fine-tuning of TRAF2 activity leads to excessive NF-kB activation, driving chronic inflammation and autoimmunity. Although TRAF2 can act as a tumor suppressor, it is predominantly described as a tumor promoter, as its expression has been correlated with increased metastatic potential and poorer prognosis in several types of cancer. Targeting TRAF2 or TRAF2-dependent signaling pathways might represent a promising anti-cancer therapeutic strategy.

Indexed as

InflammationNeoplasmsTNF Receptor-Associated Factor 2AnimalsCell SurvivalHumansNF-kappa BSignal TransductionNF-kappa BTNF Receptor-Associated Factor 2

Identifiers

PMID40229245
PMCPMC11997178

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Registered trials

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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.