Evidence mapPaperPMID 39201357Full record

ArticleInternational journal of molecular sciences2024

Mechanisms of Cell Death Induced by Erastin in Human Ovarian Tumor Cells.

Birandra K Sinha, Carri Murphy, Shalyn M Brown, Brian B Silver, Erik J Tokar, Carl D Bortner

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

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

9 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Ferroptosis in Toxicology: Present and Future.International journal of molecular sciences · 2025
    Review
  5. Ferroptosis in Cancer: Mechanism and Therapeutic Potential.International journal of molecular sciences · 2025
    Review
  6. Article
  7. Review
  8. Review
  9. Article
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

6 authors.

Birandra K SinhaMechanistic Toxicology Branch, Division of Translational Toxicology, National Institutes of Environmental Health, NIH, Research Triangle Park, NC 27709, USA.
Carri MurphyMechanistic Toxicology Branch, Division of Translational Toxicology, National Institutes of Environmental Health, NIH, Research Triangle Park, NC 27709, USA.
Shalyn M BrownMechanistic Toxicology Branch, Division of Translational Toxicology, National Institutes of Environmental Health, NIH, Research Triangle Park, NC 27709, USA.
Brian B SilverMechanistic Toxicology Branch, Division of Translational Toxicology, National Institutes of Environmental Health, NIH, Research Triangle Park, NC 27709, USA.
Erik J TokarMechanistic Toxicology Branch, Division of Translational Toxicology, National Institutes of Environmental Health, NIH, Research Triangle Park, NC 27709, USA.ORCID 0000-0002-1668-2830
Carl D BortnerLaboratory of Signal Transduction, National Institutes of Environmental Health, NIH, Research Triangle Park, NC 27709, USA.ORCID 0000-0002-5444-6628

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Erastin (ER) induces cell death through the formation of reactive oxygen species (ROS), resulting in ferroptosis. Ferroptosis is characterized by an accumulation of ROS within the cell, leading to an iron-dependent oxidative damage-mediated cell death. ER-induced ferroptosis may have potential as an alternative for ovarian cancers that have become resistant due to the presence of Ras mutation or multi-drug resistance1 (MDR1) gene expression. We used K-Ras mutant human ovarian tumor OVCAR-8 and NCI/ADR-RES, P-glycoprotein-expressing cells, to study the mechanisms of ER-induced cell death. We used these cell lines as NCI/ADR-RES cells also overexpresses superoxide dismutase, catalase, glutathione peroxidase, and transferase compared to OVCAR-8 cells, leading to the detoxification of reactive oxygen species. We found that ER was similarly cytotoxic to both cells. Ferrostatin, an inhibitor of ferroptosis, reduced ER cytotoxicity. In contrast, RSL3 (RAS-Selective Ligand3), an inducer of ferroptosis, markedly enhanced ER cytotoxicity in both cells. More ROS was detected in OVCAR-8 cells than NCI/ADR-RES cells, causing more malondialdehyde (MDA) formation in OVCAR-8 cells than in NCI/ADR-RES cells. RSL3, which was more cytotoxic to NCI/ADR-RES cells, significantly enhanced MDA formation in both cells, suggesting that glutathione peroxidase 4 (

Indexed as

FerroptosisOvarian NeoplasmsPiperazinesReactive Oxygen SpeciesAntineoplastic AgentsCarbolinesCell DeathCell Line, TumorFemaleHumansAntineoplastic AgentsCarbolineserastinPiperazinesReactive Oxygen SpeciesRSL3 compounderastinferroptosisovarian tumor cellsreactive oxygen speciesRSL3

Identifiers

PMID39201357
PMCPMC11355013

What Socratic holds

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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 Socratic graph.