Evidence map›Paper›PMID 28667123›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2017

Mutant p53 potentiates the oncogenic effects of insulin by inhibiting the tumor suppressor DAB2IP.

Elena Valentino, Arianna Bellazzo, Giulio Di Minin, Daria Sicari, Mattia Apollonio, Giosuè Scognamiglio, Maurizio Di Bonito, Gerardo Botti, Giannino Del Sal, Licio Collavin

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.5field-weighted citation impact, top 9% 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

38 citing papers in PubMed, 54 citations in OpenAlex.

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  4. DNA Damage and Repair in Pancreatic Cancer-The Latest Findings.International journal of molecular sciences · 2025
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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 4 institutions in 2 countries.

Elena ValentinoLaboratorio Nazionale Consorzio Interuniversitario Biotecnologie, 34149 Trieste, Italy.
Arianna BellazzoLaboratorio Nazionale Consorzio Interuniversitario Biotecnologie, 34149 Trieste, Italy.
Giulio Di MininInstitute of Molecular Health Sciences, Swiss Federal Institute of Technology Hoenggerberg, 8093 Zurich, Switzerland.
Daria SicariLaboratorio Nazionale Consorzio Interuniversitario Biotecnologie, 34149 Trieste, Italy.
Mattia ApollonioLaboratorio Nazionale Consorzio Interuniversitario Biotecnologie, 34149 Trieste, Italy.
Giosuè ScognamiglioDepartment of Pathology, National Cancer Institute Fondazione G. Pascale, 80131 Naples, Italy.
Maurizio Di BonitoDepartment of Pathology, National Cancer Institute Fondazione G. Pascale, 80131 Naples, Italy.
Gerardo BottiDepartment of Pathology, National Cancer Institute Fondazione G. Pascale, 80131 Naples, Italy.
Giannino Del SalLaboratorio Nazionale Consorzio Interuniversitario Biotecnologie, 34149 Trieste, Italy; delsal@lncib.it collavin@lncib.it.
Licio CollavinLaboratorio Nazionale Consorzio Interuniversitario Biotecnologie, 34149 Trieste, Italy; delsal@lncib.it collavin@lncib.it.ORCID 0000-0001-6815-5381
University of Trieste · ITIstituto Nazionale Tumori IRCCS "Fondazione G. Pascale" · ITConsorzio Interuniversitario per le Biotecnologie · ITÉcole Polytechnique Fédérale de Lausanne · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Obesity and type 2 diabetes are significant risk factors for malignancies, being associated with chronic inflammation and hyperinsulinemia. In this context, insulin can synergize with inflammation to promote proliferation, survival, and dissemination of cancer cells. Point mutation of p53 is a frequent event and a significant factor in cancer development and progression. Mutant p53 protein(s) (mutp53) can acquire oncogenic properties that increase metastasis, proliferation, and cell survival. We report that breast and prostate cancer cells with mutant p53 respond to insulin stimulation by increasing cell proliferation and invasivity, and that such a response depends on the presence of mutp53. Mechanistically, we find that mutp53 augments insulin-induced AKT1 activation by binding and inhibiting the tumor suppressor DAB2IP (DAB2-interacting protein) in the cytoplasm. This molecular axis reveals a specific gain of function for mutant p53 in the response to insulin stimulation, offering an additional perspective to understand the relationship between hyperinsulinemia and cancer evolution.

Indexed as

MutationAnimalsBreast NeoplasmsCell Line, TumorCell ProliferationCell SurvivalDiabetes ComplicationsDiabetes MellitusDisease ProgressionFemaleHumansHyperinsulinismInflammationInsulinMaleMiceAKT1 protein, humanDAB2IP protein, humanInsulinMutant ProteinsProto-Oncogene Proteins c-aktras GTPase-Activating ProteinsTP53 protein, humanTumor Suppressor Protein p53AIP1AKThyperinsulinemiamutant p53obesity

Identifiers

PMID28667123
PMCPMC5530663
OpenAlexW2724422518

What OpenQuestion holds

Textmetadata
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.