Evidence map›Paper›PMID 28154184›Full record

ArticleThe Journal of biological chemistry2017

Bax/Bak-independent mitochondrial depolarization and reactive oxygen species induction by sorafenib overcome resistance to apoptosis in renal cell carcinoma.

Bernhard Gillissen, Anja Richter, Antje Richter, Robert Preissner, Klaus Schulze-Osthoff, Frank Essmann, Peter T Daniel

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2017. 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
3.1field-weighted citation impact, top 8% 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, 50 citations in OpenAlex.

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  12. [Effect of small interfering RNA-mediated BIRC6 silencing on apoptosis and autophagy of renal cancer 786-O cells].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020
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  13. BAX-dependent mitochondrial pathway mediates the crosstalk between ferroptosis and apoptosis.Apoptosis : an international journal on programmed cell death · 2020
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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

7 authors at 4 institutions in 1 country.

Bernhard GillissenFrom the Department of Hematology, Oncology, and Tumor Immunology, University Medical Center Charité, Campus Berlin-Buch, Humboldt University, Berlin, Germany.
Anja RichterFrom the Department of Hematology, Oncology, and Tumor Immunology, University Medical Center Charité, Campus Berlin-Buch, Humboldt University, Berlin, Germany.
Antje RichterFrom the Department of Hematology, Oncology, and Tumor Immunology, University Medical Center Charité, Campus Berlin-Buch, Humboldt University, Berlin, Germany.
Robert Preissnerthe Institute of Physiology and Experimental Clinical Research Center, University Medical Center Charité, 13125 Berlin, Germany.
Klaus Schulze-Osthoffthe German Cancer Consortium and German Cancer Research Center, Im Neuenheimer Feld, 69120 Heidelberg, Germany.
Frank Essmannthe German Cancer Consortium and German Cancer Research Center, Im Neuenheimer Feld, 69120 Heidelberg, Germany.
Peter T DanielFrom the Department of Hematology, Oncology, and Tumor Immunology, University Medical Center Charité, Campus Berlin-Buch, Humboldt University, Berlin, Germany, pdaniel@mdc-berlin.de.
Heidelberg University · DEHumboldt-Universität zu Berlin · DECharité - Universitätsmedizin Berlin · DEGerman Cancer Research Center · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal cell carcinoma (RCC) is polyresistant to chemo- and radiotherapy and biologicals, including TNF-related apoptosis-inducing ligand (TRAIL). Sorafenib, a multikinase inhibitor approved for the treatment of RCC, has been shown to sensitize cancer cells to TRAIL-induced apoptosis, in particular by down-regulation of the Bak-inhibitory Bcl-2 family protein Mcl-1. Here we demonstrate that sorafenib overcomes TRAIL resistance in RCC by a mechanism that does not rely on Mcl-1 down-regulation. Instead, sorafenib induces rapid dissipation of the mitochondrial membrane potential (ΔΨ

Indexed as

Drug Resistance, NeoplasmApoptosisbcl-2-Associated X Proteinbcl-2 Homologous Antagonist-Killer ProteinCarcinoma, Renal CellCaspase 8Cell Line, TumorDown-RegulationEnzyme ActivationFlow CytometryHumansKidney NeoplasmsMembrane Potential, MitochondrialMitochondriaMyeloid Cell Leukemia Sequence 1 ProteinNiacinamideBAK1 protein, humanBAX protein, humanbcl-2-Associated X Proteinbcl-2 Homologous Antagonist-Killer ProteinCASP8 protein, humanCaspase 8MCL1 protein, humanMyeloid Cell Leukemia Sequence 1 ProteinNiacinamidePhenylurea CompoundsReactive Oxygen SpeciesRNA, Small InterferingSorafenibTNF-Related Apoptosis-Inducing LigandTNFSF10 protein, humanapoptosisBakBaxB cell lymphoma 2 (Bcl-2) familycancerdrug resistancereactive oxygen species (ROS)sorafenibTrail

Identifiers

PMID28154184
PMCPMC5399102
OpenAlexW2584838045

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.