Evidence map›Paper›PMID 23610071›Full record

ArticleEMBO molecular medicine2013

Stathmin regulates mutant p53 stability and transcriptional activity in ovarian cancer.

Maura Sonego, Monica Schiappacassi, Sara Lovisa, Alessandra Dall'Acqua, Marina Bagnoli, Francesca Lovat, Massimo Libra, Sara D'Andrea, Vincenzo Canzonieri, Loredana Militello and 11 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

34 citing papers in PubMed, 53 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. International journal of molecular sciences · 2024
    Article
  5. Article
  6. International journal of molecular sciences · 2023
    Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. STMN1 and MKI67 Are Upregulated in Uterine Leiomyosarcoma and Are Potential Biomarkers for its Diagnosis.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Article
  14. Cancer Stemness: p53 at the Wheel.Frontiers in oncology · 2020
    Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

21 authors at 7 institutions in 2 countries.

Maura SonegoDivision of Experimental Oncology 2, Centro di Riferimento Oncologico, National Cancer Institute, Aviano, Italy.
Monica Schiappacassi
Sara Lovisa
Alessandra Dall'Acqua
Marina Bagnoli
Francesca Lovat
Massimo Libra
Sara D'Andrea
Vincenzo Canzonieri
Loredana Militello
Marco Napoli
Giorgio Giorda
Barbara Pivetta
Delia Mezzanzanica
Mattia Barbareschi
Barbara Valeri
Silvana Canevari
Alfonso Colombatti
Barbara Belletti
Giannino Del Sal
Gustavo Baldassarre
Centro di Riferimento Oncologico · ITFondazione IRCCS Istituto Nazionale dei Tumori · ITAREA Science Park · ITOspedale Santa Chiara · ITThe University of Texas MD Anderson Cancer Center · USUniversity of Catania · ITUniversity of Udine · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Stathmin is a p53-target gene, frequently overexpressed in late stages of human cancer progression. Type II High Grade Epithelial Ovarian Carcinomas (HG-EOC) represents the only clear exception to this observation. Here, we show that stathmin expression is necessary for the survival of HG-EOC cells carrying a p53 mutant (p53(MUT) ) gene. At molecular level, stathmin favours the binding and the phosphorylation of p53(MUT) by DNA-PKCS , eventually modulating p53(MUT) stability and transcriptional activity. Inhibition of stathmin or DNA-PKCS impaired p53(MUT) -dependent transcription of several M phase regulators, resulting in M phase failure and EOC cell death, both in vitro and in vivo. In primary human EOC a strong correlation exists between stathmin, DNA-PKCS , p53(MUT) overexpression and its transcriptional targets, further strengthening the relevance of the new pathway here described. Overall our data support the hypothesis that the expression of stathmin and p53 could be useful for the identification of high risk patients that will benefit from a therapy specifically acting on mitotic cancer cells.

Indexed as

AnimalsAntineoplastic AgentsApoptosisCalcium-Binding ProteinsCell Cycle CheckpointsCell SurvivalFemaleHumansMiceMutationOvarian NeoplasmsPhosphorylationProtein BindingProtein StabilityRNA InterferenceRNA, Small InterferingAntineoplastic AgentsCalcium-Binding ProteinsCIB1 protein, humanRNA, Small InterferingStathminTumor Suppressor Protein p53

Identifiers

PMID23610071
PMCPMC3662314
OpenAlexW2097171599

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.