Evidence map›Paper›PMID 31462745›Full record

ArticleScientific reports2019

Expression profiles of p53/p73, NME and GLI families in metastatic melanoma tissue and cell lines.

Petar Ozretić, Nikolina Hanžić, Bastien Proust, Maja Sabol, Diana Trnski, Martina Radić, Vesna Musani, Yari Ciribilli, Ivan Milas, Zvonimir Puljiz and 3 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

21 citing papers in PubMed, 27 citations in OpenAlex.

  1. Trial
  2. The p53 Isoforms as Potential Biomarkers in Different Cancer Entities.International journal of molecular sciences · 2026
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  13. p53 Family in Resistance to Targeted Therapy of Melanoma.International journal of molecular sciences · 2022
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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

13 authors at 3 institutions in 2 countries.

Petar OzretićDivision of Molecular Medicine, Ruđer Bošković Institute, Bijenička cesta 54, HR-10000, Zagreb, Croatia.ORCID http://orcid.org/0000-0001-9757-6636
Nikolina HanžićDivision of Molecular Medicine, Ruđer Bošković Institute, Bijenička cesta 54, HR-10000, Zagreb, Croatia.
Bastien ProustDivision of Molecular Medicine, Ruđer Bošković Institute, Bijenička cesta 54, HR-10000, Zagreb, Croatia.
Maja SabolDivision of Molecular Medicine, Ruđer Bošković Institute, Bijenička cesta 54, HR-10000, Zagreb, Croatia.
Diana TrnskiDivision of Molecular Medicine, Ruđer Bošković Institute, Bijenička cesta 54, HR-10000, Zagreb, Croatia.
Martina RadićDivision of Molecular Medicine, Ruđer Bošković Institute, Bijenička cesta 54, HR-10000, Zagreb, Croatia.
Vesna MusaniDivision of Molecular Medicine, Ruđer Bošković Institute, Bijenička cesta 54, HR-10000, Zagreb, Croatia.ORCID http://orcid.org/0000-0001-9927-3727
Yari CiribilliDepartment of Cellular, Computational and Integrative Biology (CIBIO), University of Trento, Via Sommarive 9, Povo (Trento), IT-38123, Italy.ORCID http://orcid.org/0000-0001-9231-379X
Ivan MilasSestre milosrdnice University Hospital Center, Vinogradska cesta 29, HR-10000, Zagreb, Croatia.
Zvonimir PuljizSestre milosrdnice University Hospital Center, Vinogradska cesta 29, HR-10000, Zagreb, Croatia.
Maja Herak BosnarDivision of Molecular Medicine, Ruđer Bošković Institute, Bijenička cesta 54, HR-10000, Zagreb, Croatia.
Sonja LevanatDivision of Molecular Medicine, Ruđer Bošković Institute, Bijenička cesta 54, HR-10000, Zagreb, Croatia.
Neda SladeDivision of Molecular Medicine, Ruđer Bošković Institute, Bijenička cesta 54, HR-10000, Zagreb, Croatia. slade@irb.hr.ORCID http://orcid.org/0000-0003-3620-3099
Ruđer Bošković Institute · HRSisters of Charity Hospital · HRUniversity of Trento · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Unlike other tumours, TP53 is rarely mutated in melanoma; however, it fails to function as a tumour suppressor. We assume that its functions might be altered through interactions with several families of proteins, including p53/p73, NME and GLI. To elucidate the potential interplay among these families we analysed the expression profiles of aforementioned genes and proteins in a panel of melanoma cell lines, metastatic melanoma specimens and healthy corresponding tissue. Using qPCR a higher level of NME1 gene expression and lower levels of Δ40p53β, ΔNp73, GLI1, GLI2 and PTCH1 were observed in tumour samples compared to healthy tissue. Protein expression of Δ133p53α, Δ160p53α and ΔNp73α isoforms, NME1 and NME2, and N'ΔGLI1, GLI1FL, GLI2ΔN isoforms was elevated in tumour tissue, whereas ∆Np73β was downregulated. The results in melanoma cell lines, in general, support these findings. In addition, we correlated expression profiles with clinical features and outcome. Higher Δ133p53β and p53α mRNA and both GLI1 mRNA and GLI3R protein expression had a negative impact on the overall survival. Shorter overall survival was also connected with lower p53β and NME1 gene expression levels. In conclusion, all examined genes may have implications in melanoma development and functional inactivity of TP53.

Indexed as

Gene Expression Regulation, NeoplasticCell Line, TumorDisease-Free SurvivalFemaleHumansMaleMelanomaNeoplasm MetastasisNucleoside-Diphosphate KinaseSurvival RateTumor Protein p73Tumor Suppressor Protein p53Nucleoside-Diphosphate KinaseTP53 protein, humanTP73 protein, humanTumor Protein p73Tumor Suppressor Protein p53

Identifiers

PMID31462745
PMCPMC6713730
OpenAlexW2970774940

What OpenQuestion holds

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LicenceCC BY
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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.