Evidence map›Paper›PMID 26986846›Full record

ArticleOncology reports2016

PRIMA-1MET induces apoptosis through accumulation of intracellular reactive oxygen species irrespective of p53 status and chemo-sensitivity in epithelial ovarian cancer cells.

Nobuhisa Yoshikawa, Hiroaki Kajiyama, Kae Nakamura, Fumi Utsumi, Kaoru Niimi, Hiroko Mitsui, Ryuichiro Sekiya, Shiro Suzuki, Kiyosumi Shibata, David Callen and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

25 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. Mechanisms of apoptosis-related non-coding RNAs in ovarian cancer: a narrative review.Apoptosis : an international journal on programmed cell death · 2025
    Review
  4. Article
  5. PRIMA-1ACS omega · 2023
    Article
  6. The p53 reactivator PRIMA-1Investigational new drugs · 2023
    Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. PRIMA‑1Oncology reports · 2021
    Article
  16. Article
  17. Review
  18. Article
  19. Synergistic effects of PRIMA-1Haematologica · 2020
    Article
  20. Review
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 at 2 institutions in 2 countries.

Nobuhisa YoshikawaDepartment of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Hiroaki KajiyamaDepartment of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Kae NakamuraDepartment of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Fumi UtsumiDepartment of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Kaoru NiimiDepartment of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Hiroko MitsuiDepartment of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Ryuichiro SekiyaDepartment of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Shiro SuzukiDepartment of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Kiyosumi ShibataDepartment of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
David CallenCentre for Personalized Cancer Medicine, Discipline of Medicine, University of Adelaide, Adelaide, SA, Australia.
Fumitaka KikkawaDepartment of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Nagoya University · JPUniversity of Adelaide · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There is an intensive need for the development of novel drugs for the treatment of epithelial ovarian cancer (EOC), the most lethal gynecologic malignancy due to the high recurrence rate. TP53 mutation is a common event in EOC, particularly in high-grade serous ovarian cancer, where it occurs in more than 90% of cases. Recently, PRIMA-1 and PRIMA‑1MET (p53 reactivation and induction of massive apoptosis and its methylated form) were shown to have an antitumor effect on several types of cancer. Despite that PRIMA-1MET is the first compound evaluated in clinical trials, the antitumor effects of PRIMA-1MET on EOC remain unclear. In this study, we investigated the therapeutic potential of PRIMA-1MET for the treatment of EOC cells. PRIMA-1MET treatment of EOC cell lines (n=13) resulted in rapid apoptosis at various concentrations (24 h IC50 2.6-20.1 µM). The apoptotic response was independent of the p53 status and chemo-sensitivity. PRIMA‑1MET treatment increased intracellular reactive oxygen species (ROS), and PRIMA-1MET-induced apoptosis was rescued by an ROS scavenger. Furthermore, RNA expression analysis revealed that the mechanism of action of PRIMA‑1MET may be due to inhibition of antioxidant enzymes, such as Prx3 and GPx-1. In conclusion, our results suggest that PRIMA-1MET represents a novel therapeutic strategy for the treatment of ovarian cancer irrespective of p53 status and chemo-sensitivity.

Indexed as

Antineoplastic AgentsApoptosisCarcinoma, Ovarian EpithelialCell Line, TumorDrug Resistance, NeoplasmDrug Screening Assays, AntitumorFemaleHumansNeoplasms, Glandular and EpithelialOvarian NeoplasmsPoly (ADP-Ribose) Polymerase-1ProteolysisQuinuclidinesReactive Oxygen SpeciesTumor Suppressor Protein p53Antineoplastic AgentseprenetapoptPARP1 protein, humanPoly (ADP-Ribose) Polymerase-1QuinuclidinesReactive Oxygen SpeciesTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID26986846
PMCPMC4811399
OpenAlexW2290932118

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.