Evidence map›Paper›PMID 32144381›Full record

ArticleCell death and differentiation2020

Fenretinide induces a new form of dynamin-dependent cell death in pediatric sarcoma.

Eva Brack, Marco Wachtel, Anja Wolf, Andres Kaech, Urs Ziegler, Beat W Schäfer

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Targeting ferroptosis in osteosarcoma.Journal of bone oncology · 2021
    Review
  11. Article
  12. 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

6 authors at 2 institutions in 1 country.

Eva BrackDepartment of Oncology and Children's Research Center, University Children's Hospital Zurich, Zurich, Switzerland.
Marco WachtelDepartment of Oncology and Children's Research Center, University Children's Hospital Zurich, Zurich, Switzerland.
Anja WolfDepartment of Oncology and Children's Research Center, University Children's Hospital Zurich, Zurich, Switzerland.
Andres KaechCenter for Microscopy and Image Analysis, University of Zurich, Zurich, Switzerland.
Urs ZieglerCenter for Microscopy and Image Analysis, University of Zurich, Zurich, Switzerland.
Beat W SchäferDepartment of Oncology and Children's Research Center, University Children's Hospital Zurich, Zurich, Switzerland. beat.schaefer@kispi.uzh.ch.ORCID http://orcid.org/0000-0001-5988-2915
University Children's Hospital Zurich · CHUniversity of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alveolar rhabdomyosarcoma (aRMS) is a highly malicious childhood malignancy characterized by specific chromosomal translocations mostly encoding the oncogenic transcription factor PAX3-FOXO1 and therefore also referred to as fusion-positive RMS (FP-RMS). Previously, we have identified fenretinide (retinoic acid p-hydroxyanilide) to affect PAX3-FOXO1 expression levels as well as FP-RMS cell viability. Here, we characterize the mode of action of fenretinide in more detail. First, we demonstrate that fenretinide-induced generation of reactive oxygen species (ROS) depends on complex II of the mitochondrial respiratory chain, since ROS scavenging as well as complexing of iron completely abolished cell death. Second, we co-treated cells with a range of pharmacological inhibitors of specific cell death pathways including z-vad (apoptosis), necrostatin-1 (necroptosis), 3-methyladenine (3-MA) (autophagy), and ferrostatin-1 (ferroptosis) together with fenretinide. Surprisingly, none of these inhibitors was able to prevent cell death. Also genetic depletion of key players in the apoptotic and necroptotic pathway (BAK, BAX, and RIPK1) confirmed the pharmacological data. Interestingly however, electron microscopy of fenretinide-treated cells revealed an excessive accumulation of cytoplasmic vacuoles, which were distinct from autophagosomes. Further flow cytometry and fluorescence microscopy experiments suggested a hyperstimulation of macropinocytosis, leading to an accumulation of enlarged early and late endosomes. Surprisingly, pharmacological inhibition as well as genetic depletion of large dynamin GTPases completely abolished fenretinide-induced vesicle formation and subsequent cell death, suggesting a new form of dynamin-dependent programmed cell death. Taken together, our data identify a new form of cell death mediated through the production of ROS by fenretinide treatment, highlighting the value of this compound for treatment of sarcoma patients including FP-RMS.

Indexed as

Cell DeathCell Line, TumorCell SurvivalChildCytoplasmic VesiclesDynaminsElectron Transport Complex IIEndosomesFenretinideGene Expression Regulation, NeoplasticHumansMitochondriaReactive Oxygen SpeciesRNA, MessengerSarcomaDynaminsElectron Transport Complex IIFenretinideReactive Oxygen SpeciesRNA, Messenger

Identifiers

PMID32144381
PMCPMC7370225
OpenAlexW3009156531

What OpenQuestion holds

Textmetadata
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.