Evidence map›Paper›PMID 36672272›Full record

ArticleCells2023

Erk1/2-Dependent HNSCC Cell Susceptibility to Erastin-Induced Ferroptosis.

Dragana Savic, Teresa Bernadette Steinbichler, Julia Ingruber, Giulia Negro, Bertram Aschenbrenner, Herbert Riechelmann, Ute Ganswindt, Sergej Skvortsov, József Dudás, Ira-Ida Skvortsova

Open access · goldAbstract read
In one paragraph

Article in Cells, 2023. 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
3.9field-weighted citation impact, top 6% 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

9 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Unveiling therapeutic avenues targeting xCT in head and neck cancer.Cellular oncology (Dordrecht, Netherlands) · 2024
    Review
  6. Article
  7. Article
  8. Article
  9. 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

10 authors at 2 institutions in 1 country.

Dragana SavicLaboratory for Experimental and Translational Research on Radiation Oncology (EXTRO-Lab), Department of Therapeutic Radiology and Oncology, Medical University of Innsbruck, A-6020 Innsbruck, Austria.ORCID 0000-0001-5196-4676
Teresa Bernadette SteinbichlerDepartment of Otorhinolaryngology and Head and Neck Surgery, Medical University of Innsbruck, A-6020 Innsbruck, Austria.
Julia IngruberDepartment of Otorhinolaryngology and Head and Neck Surgery, Medical University of Innsbruck, A-6020 Innsbruck, Austria.
Giulia NegroLaboratory for Experimental and Translational Research on Radiation Oncology (EXTRO-Lab), Department of Therapeutic Radiology and Oncology, Medical University of Innsbruck, A-6020 Innsbruck, Austria.
Bertram AschenbrennerDepartment of Dermatology, Medical University of Vienna, A-1090 Vienna, Austria.
Herbert RiechelmannDepartment of Otorhinolaryngology and Head and Neck Surgery, Medical University of Innsbruck, A-6020 Innsbruck, Austria.
Ute GanswindtDepartment of Therapeutic Radiology and Oncology, A-6020 Innsbruck, Austria.
Sergej SkvortsovLaboratory for Experimental and Translational Research on Radiation Oncology (EXTRO-Lab), Department of Therapeutic Radiology and Oncology, Medical University of Innsbruck, A-6020 Innsbruck, Austria.
József DudásDepartment of Otorhinolaryngology and Head and Neck Surgery, Medical University of Innsbruck, A-6020 Innsbruck, Austria.ORCID 0000-0002-9877-3399
Ira-Ida SkvortsovaLaboratory for Experimental and Translational Research on Radiation Oncology (EXTRO-Lab), Department of Therapeutic Radiology and Oncology, Medical University of Innsbruck, A-6020 Innsbruck, Austria.ORCID 0000-0001-8993-611X
Innsbruck Medical University · ATMedical University of Vienna · AT

Funding

Austrian Science Fund FWF I 4140Austrian Science Fund FWF P 36528
6 · The paper itself

Abstract

Unfavorable clinical outcomes mean that cancer researchers must attempt to develop novel therapeutic strategies to overcome therapeutic resistance in patients with HNSCC. Recently, ferroptosis was shown to be a promising pathway possessing druggable targets, such as xCT (SLC7A11). Unfortunately, little is known about the molecular mechanisms underlying the susceptibility of HNSCC cells to ferroptosis. The goal of this study was to determine whether HNSCC cells with activated Erk1/2 are vulnerable to ferroptosis induction. Our results have shown that xCT (SLC7A11) was overexpressed in malignant tissues obtained from the patients with HNSCC, whereas normal mucosa demonstrated weak expression of the protein. In order to investigate the role of Erk1/2 in the decrease in cell viability caused by erastin, xCT-overexpressing FaDu and SCC25 HNSCC cells were used. The ravoxertinib-dependent inhibition of Erk1/2 signaling led to the decrease in erastin efficacy due to the effect on ROS production and the upregulation of ROS scavengers SOD1 and SOD2, resulting in repressed lipid peroxidation. Therefore, it was concluded that the erastin-dependent activation of ferroptosis seems to be a promising approach which can be further developed as an additional strategy for the treatment of HNSCC. As ferroptosis induction via erastin is strongly dependent on the expression of Erk1/2, this MAP kinase can be considered as a predictor for cancer cells' response to erastin.

Indexed as

FerroptosisHead and Neck NeoplasmsHumansPiperazinesReactive Oxygen SpeciesSquamous Cell Carcinoma of Head and NeckerastinPiperazinesReactive Oxygen SpecieserastinERK signalingHNSCCxCT

Identifiers

PMID36672272
PMCPMC9856753
OpenAlexW4316468260

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.