Evidence map›Paper›PMID 25277184›Full record

ArticleOncotarget2014

TRIM8 anti-proliferative action against chemo-resistant renal cell carcinoma.

Mariano Francesco Caratozzolo, Alessio Valletti, Margherita Gigante, Italia Aiello, Francesca Mastropasqua, Flaviana Marzano, Pasquale Ditonno, Giuseppe Carrieri, Hélène Simonnet, Anna Maria D'Erchia and 4 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

37 citing papers in PubMed, 46 citations in OpenAlex.

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  20. Rise of TRIM8: A Molecule of Duality.Molecular therapy. Nucleic acids · 2020
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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

14 authors at 5 institutions in 2 countries.

Mariano Francesco CaratozzoloInstitute for Biomedical Technologies ITB, Bari, Italy. Contributed equally to this work.
Alessio VallettiInstitute of Biomembranes and Bioenergetics IBBE, Bari, Italy. Contributed equally to this work.
Margherita GiganteDept Biomedical Science, University of Foggia, Foggia, Italy.
Italia AielloDept Biosciences, Biotechnologies and Biopharmaceutics, University of Bari "A. Moro", Bari, Italy.
Francesca MastropasquaDept Biosciences, Biotechnologies and Biopharmaceutics, University of Bari "A. Moro", Bari, Italy.
Flaviana MarzanoInstitute for Biomedical Technologies ITB, Bari, Italy.
Pasquale DitonnoDept Emergency and Organ Transplantation DETO, University of Bari "A. Moro", Bari, Italy.
Giuseppe CarrieriDept Surgical Science, University of Foggia, Foggia, Italy.
Hélène SimonnetCentre de Recherche en Cancérologie de Lyon, Faculté de Médecine Lyon-Est, LYON Cedex 08 France.
Anna Maria D'ErchiaDept Biosciences, Biotechnologies and Biopharmaceutics, University of Bari "A. Moro", Bari, Italy.
Elena RanieriDept Biomedical Science, University of Foggia, Foggia, Italy.
Graziano PesoleInstitute of Biomembranes and Bioenergetics IBBE, Bari, Italy. Dept Biosciences, Biotechnologies and Biopharmaceutics, University of Bari "A. Moro", Bari, Italy.
Elisabetta SbisàInstitute for Biomedical Technologies ITB, Bari, Italy.
Apollonia TulloInstitute for Biomedical Technologies ITB, Bari, Italy.
Institute of Biomedical Technologies · ITUniversity of Bari Aldo Moro · ITUniversity of Foggia · ITInstitute of Biomembranes, Bioenergetics and Molecular Biotechnologies · ITCentre de Recherche en Cancérologie de Lyon · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In some tumours, despite a wild-type p53 gene, the p53 pathway is inactivated by alterations in its regulators or by unknown mechanisms, leading to resistance to cytotoxic therapies. Understanding the mechanisms of functional inactivation of wild-type p53 in these tumours may help to define prospective targets for treating cancer by restoring p53 activity. Recently, we identified TRIM8 as a new p53 modulator, which stabilizes p53 impairing its association with MDM2 and inducing the reduction of cell proliferation. In this paper we demonstrated that TRIM8 deficit dramatically impairs p53-mediated cellular responses to chemotherapeutic drugs and that TRIM8 is down regulated in patients affected by clear cell Renal Cell Carcinoma (ccRCC), an aggressive drug-resistant cancer showing wild-type p53. These results suggest that down regulation of TRIM8 might be an alternative way to suppress p53 activity in RCC. Interestingly, we show that TRIM8 expression recovery in RCC cell lines renders these cells sensitive to chemotherapeutic treatments following p53 pathway re-activation. These findings provide the first mechanistic link between TRIM8 and the drug resistance of ccRCC and suggest more generally that TRIM8 could be used as enhancer of the chemotherapy efficacy in cancers where p53 is wild-type and its pathway is defective.

Indexed as

AgedAged, 80 and overBlotting, WesternCarcinoma, Renal CellCarrier ProteinsCell Line, TumorCell ProliferationDrug Resistance, NeoplasmFemaleHumansImmunoprecipitationKidney NeoplasmsMaleMiddle AgedNerve Tissue ProteinsReverse Transcriptase Polymerase Chain ReactionCarrier ProteinsNerve Tissue ProteinsTRIM8 protein, humanTumor Suppressor Protein p53

Identifiers

PMID25277184
PMCPMC4202135
OpenAlexW2139236599

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.