Evidence map›Paper›PMID 40878805›Full record

ArticleCarcinogenesis2025

Δ133p53 isoform enhances TLR4 function to promote tumor growth.

Sasini Polwatta Lekamlage, Alexandra N Boix De Jesus, Adriana Machado Saraiva, Catherine Drummond, Harrison Dolan, Francesc March de Ribot, Janice A Royds, Sunali Mehta, Antony W Braithwaite, Noelyn A Hung and 1 more

Abstract read
In one paragraph

Article in Carcinogenesis, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

11 authors.

Sasini Polwatta LekamlageDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin 9016, New Zealand.
Alexandra N Boix De JesusDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin 9016, New Zealand.
Adriana Machado SaraivaDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin 9016, New Zealand.
Catherine DrummondDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin 9016, New Zealand.
Harrison DolanDepartment of Medical Laboratory Science, School of Pharmacy, University of Otago, Dunedin 9016, New Zealand.
Francesc March de RibotDepartment of Medicine, Dunedin School of Medicine, University of Otago, Dunedin 9016, New Zealand.ORCID 0000-0002-9438-4740
Janice A RoydsDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin 9016, New Zealand.
Sunali MehtaDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin 9016, New Zealand.ORCID 0000-0002-1777-1245
Antony W BraithwaiteDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin 9016, New Zealand.ORCID 0000-0002-8671-5036
Noelyn A HungDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin 9016, New Zealand.ORCID 0000-0002-2401-9764
Tania L SlatterDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin 9016, New Zealand.ORCID 0000-0003-4031-0604

Funding

Marsden FundRoyal Society of New Zealand 18-UOO-089
6 · The paper itself

Abstract

Tumor protein 53 (TP53) acts as a tumor suppressor and is often mutated in cancer. Isoforms of TP53, such as the Δ133p53 family, can promote tumor growth and metastasis. Therefore, targeting Δ133p53 function may represent a new strategy for preventing tumor metastasis. To inform the identification of proteins to target in Δ133p53-expressing tumors, changes at the cell surface were characterized. Inhibition of cell surface trafficking in a mouse model syngrafted with tumors expressing proteins similar to Δ133p53 (Δ122p53) was associated with reduced tumor growth and metastasis. After confirming that changes at the cell surface were important for Δ133p53 tumor promotion, characterization of protein changes at the Δ133p53/Δ122p53 cell surface revealed increased expression of the toll-like receptor 4 (TLR4) and the TLR4 agonist, apoptosis inhibitor 5. Furthermore, inhibition of TLR4 was sufficient to reduce Δ122p53 tumor growth. Altogether, these results suggest a role for Δ133p53 in contributing to tumor progression by stimulating TLR4 function. Furthermore, targeting changes at the cell surface can reduce Δ133p53 tumor promotion.

Indexed as

NeoplasmsToll-Like Receptor 4Tumor Suppressor Protein p53AnimalsCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansMiceProtein IsoformsProtein IsoformsTlr4 protein, mouseToll-Like Receptor 4Trp53 protein, mouseTumor Suppressor Protein p53API5cancercell surfaceTLR4Δ133p53

Identifiers

PMID40878805
PMCPMC12683340

What Socratic holds

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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 Socratic graph.