Evidence map›Paper›PMID 20107899›Full record

ArticleApoptosis : an international journal on programmed cell death2010

Potential involvement of F0F1-ATP(synth)ase and reactive oxygen species in apoptosis induction by the antineoplastic agent erucylphosphohomocholine in glioblastoma cell lines : a mechanism for induction of apoptosis via the 18 kDa mitochondrial translocator protein.

Leo Veenman, Julia Alten, Karen Linnemannstöns, Yulia Shandalov, Sivan Zeno, Max Lakomek, Moshe Gavish, Wilfried Kugler

Open access · hybridAbstract read
In one paragraph

Article in Apoptosis : an international journal on programmed cell death, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

32 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
  2. Mitochondrial control of microglial phagocytosis by the translocator protein and hexokinase 2 in Alzheimer's disease.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  3. Article
  4. Article
  5. Cellular sources of TSPO expression in healthy and diseased brain.European journal of nuclear medicine and molecular imaging · 2021
    Review
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  7. Article
  8. Natural products and other inhibitors of FEuropean journal of medicinal chemistry · 2020
    Review
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  11. Article
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  19. Sifting through the surfeit of neuroinflammation tracers.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2018
    Review
  20. 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

8 authors at 4 institutions in 2 countries.

Leo VeenmanDepartment of Molecular Pharmacology, Rappaport Family Institute for Research in the Medical Sciences, Technion-Israel Institute of Technology, P.O. Box 9649, Bat-Galim, 31096, Haifa, Israel. veenmanl@techunix.technion.ac.il
Julia Alten
Karen Linnemannstöns
Yulia Shandalov
Sivan Zeno
Max Lakomek
Moshe Gavish
Wilfried Kugler
Rappaport Family Institute for Research in the Medical Sciences · ILUniversitätsmedizin Göttingen · DEZentrum für Kinderheilkunde · DETechnion – Israel Institute of Technology · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Erucylphosphohomocholine (ErPC3, Erufosine) was reported previously to induce apoptosis in otherwise highly apoptosis-resistant malignant glioma cell lines while sparing their non-tumorigenic counterparts. We also previously found that the mitochondrial 18 kDa Translocator Protein (TSPO) is required for apoptosis induction by ErPC3. These previous studies also suggested involvement of reactive oxygen species (ROS). In the present study we further investigated the potential involvement of ROS generation, the participation of the mitochondrial respiration chain, and the role of the mitochondrial F(O)F(1)-ATP(synth)ase in the pro-apoptotic effects of ErPC3 on U87MG and U118MG human glioblastoma cell lines. For this purpose, cells were treated with the ROS chelator butylated hydroxyanisole (BHA), the mitochondrial respiration chain inhibitors rotenone, antimycin A, myxothiazol, and the uncoupler CCCP. Also oligomycin and piceatannol were studied as inhibitors of the F(O) and F(1) subunits of the mitochondrial F(O)F(1)-ATP(synth)ase, respectively. BHA was able to attenuate apoptosis induction by ErPC3, including mitochondrial ROS generation as determined with cardiolipin oxidation, as well as collapse of the mitochondrial membrane potential (Deltapsi(m)). Similarly, we found that oligomycin attenuated apoptosis and collapse of the Deltapsi(m), normally induced by ErPC3, including the accompanying reductions in cellular ATP levels. Other inhibitors of the mitochondrial respiration chain, as well as piceatannol, did not show such effects. Consequently, our findings strongly point to a role for the F(O) subunit of the mitochondrial F(O)F(1)-ATP(synth)ase in ErPC3-induced apoptosis and dissipation of Deltapsi(m) as well as ROS generation by ErPC3 and TSPO.

Indexed as

ApoptosisAdenosine TriphosphateAntineoplastic AgentsBrain NeoplasmsButylated HydroxyanisoleCaspasesCell Line, TumorCyclosporineElectron TransportEnzyme InhibitorsErucic AcidsGlioblastomaHumansMembrane Potential, MitochondrialMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition Pore3,3',4,5'-tetrahydroxystilbeneAdenosine TriphosphateAntineoplastic AgentsButylated HydroxyanisoleCaspasesCyclosporineEnzyme InhibitorsErucic Acidserucylphosphohomocholine ErPC3Mitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreOligomycinsPhosphorylcholineProton-Translocating ATPasesReactive Oxygen SpeciesReceptors, GABAStilbenesTSPO protein, human

Identifiers

PMID20107899
PMCPMC3128697
OpenAlexW2086774306

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.