Evidence map›Paper›PMID 32416440›Full record

ArticleTranslational oncology2020

Redox Modulation and Induction of Ferroptosis as a New Therapeutic Strategy in Hepatocellular Carcinoma.

Jana Lippmann, Kathrin Petri, Simone Fulda, Juliane Liese

Open access · goldAbstract read
In one paragraph

Article in Translational oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.3field-weighted citation impact, top 4% 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

28 citing papers in PubMed, 56 citations in OpenAlex.

  1. Review
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  4. Article
  5. Novel Therapeutics for Hepatocellular Carcinoma.Clinics in liver disease · 2025
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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

4 authors at 4 institutions in 2 countries.

Jana LippmannInstitute for Experimental Cancer Research in Pediatrics, Goethe-University, 60528, Frankfurt, Germany; Department of Radiation Oncology, Inselspital, Bern University Hospital, Bern, Switzerland.
Kathrin PetriLaboratory of Experimental Surgery, Department of General and Thoracic Surgery, University Hospital of Giessen, Giessen Germany; Department of General and Thoracic Surgery, University Hospital of Giessen, Giessen University, Giessen, Germany.
Simone FuldaInstitute for Experimental Cancer Research in Pediatrics, Goethe-University, 60528, Frankfurt, Germany; German Cancer Consortium (DKTK), Partner Site Frankfurt, Germany; German Cancer Research Center (DKFZ), 69120, Heidelberg, Germany.
Juliane LieseInstitute for Experimental Cancer Research in Pediatrics, Goethe-University, 60528, Frankfurt, Germany; Laboratory of Experimental Surgery, Department of General and Thoracic Surgery, University Hospital of Giessen, Giessen Germany; Department of General and Thoracic Surgery, University Hospital of Giessen, Giessen University, Giessen, Germany; German Cancer Consortium (DKTK), Partner Site Frankfurt, Germany; German Cancer Research Center (DKFZ), 69120, Heidelberg, Germany. Electronic address: Juliane.liese@chiru.med.uni-giessen.de.
Deutschen Konsortium für Translationale Krebsforschung · DEGoethe University Frankfurt · DEHeidelberg University · DEUniversitätsklinikum Gießen und Marburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ferroptosis, a newly discovered form of cell death mediated by reactive oxygen species (ROS) and lipid peroxidation, has recently been shown to have an impact on various cancer types; however, so far there are only few studies about its role in hepatocellular carcinoma (HCC). The delicate equilibrium of ROS in cancer cells has found to be crucial for cell survival, thus increased levels may trigger ferroptosis in HCC. In our study, we investigated the effect of different ROS modulators and ferroptosis inducers on a human HCC cell line and a human hepatoblastoma cell line. We identified a novel synergistic cell death induction by the combination of Auranofin and buthionine sulfoxime (BSO) or by Erastin and BSO at subtoxic concentrations. We found a caspase-independent, redox-regulated cell death, which could be rescued by different inhibitors of ferroptosis. Both cotreatments stimulated lipid peroxidation. All these findings indicated ferroptotic cell death. Both cotreatments affected the canonical ferroptosis pathway through GPX4 downregulation. We also found an accumulation of Nrf2 and HO-1, indicating an additional effect on the non-canonical pathway. Our results implicate that targeting these two main ferroptotic pathways simultaneously can overcome chemotherapy resistance in HCC.

Identifiers

PMID32416440
PMCPMC7283515
OpenAlexW3024451066

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.