Evidence map›Paper›PMID 21831290›Full record

ArticleJournal of experimental & clinical cancer research : CR2011

Statin-induced apoptosis via the suppression of ERK1/2 and Akt activation by inhibition of the geranylgeranyl-pyrophosphate biosynthesis in glioblastoma.

Masashi Yanae, Masanobu Tsubaki, Takao Satou, Tatsuki Itoh, Motohiro Imano, Yuzuru Yamazoe, Shozo Nishida

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed, 2 pooled it
2.1field-weighted citation impact, top 13% 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

73 citing papers in PubMed, 2 syntheses or guidelines pooled it, 125 citations in OpenAlex.

  1. Pooled it
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  12. Glioblastoma Therapy: Past, Present and Future.International journal of molecular sciences · 2024
    Review
  13. Review
  14. Glioblastoma Metabolism: Insights and Therapeutic Strategies.International journal of molecular sciences · 2023
    Review
  15. Article
  16. Article
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13 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Masashi YanaeDivision of Pharmacotherapy, Kinki University School of Pharmacy, Kowakae, Higashi-Osaka, Japan.
Masanobu Tsubaki
Takao Satou
Tatsuki Itoh
Motohiro Imano
Yuzuru Yamazoe
Shozo Nishida
Kindai University · JPKindai University Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundStatins are inhibitors of 3-hydroxy-3-methylglutaryl-coenzyme A reductase, the rate-limiting enzyme in cholesterol synthesis. The inhibition of this key enzyme in the mevalonate pathway leads to suppression of cell proliferation and induction of apoptosis. However, the molecular mechanism of apoptosis induction by statins is not well understood in glioblastoma. In the present study, we attempted to elucidate the mechanism by which statins induce apoptosis in C6 glioma cells.

methodsThe cytotoxicity of statins toward the C6 glioma cells were evaluated using a cell viability assay. The enzyme activity of caspase-3 was determined using activity assay kits. The effects of statins on signal transduction molecules were determined by western blot analyses.

resultsWe found that statins inhibited cell proliferation and induced apoptosis in these cells. We also observed an increase in caspase-3 activity. The apoptosis induced by statins was not inhibited by the addition of farnesyl pyrophosphate, squalene, ubiquinone, and isopentenyladenine, but by geranylgeranyl-pyrophosphate (GGPP). Furthermore, statins decreased the levels of phosphorylated extracellular signal-regulated kinase 1/2 (ERK1/2) and Akt.

conclusionsThese results suggest that statins induce apoptosis when GGPP biosynthesis is inhibited and consequently decreases the level of phosphorylated ERK1/2 and Akt. The results of this study also indicate that statins could be used as anticancer agents in glioblastoma.

Indexed as

Acyl Coenzyme AApoptosisCell Growth ProcessesCell SurvivalEnzyme ActivationFemaleGlioblastomaHumansHydroxymethylglutaryl-CoA Reductase InhibitorsMaleMevalonic AcidMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3PhosphorylationPolyisoprenyl PhosphatesProto-Oncogene Proteins c-akt3-hydroxy-3-methylglutaryl-coenzyme AAcyl Coenzyme Ageranylgeranyl pyrophosphateHydroxymethylglutaryl-CoA Reductase InhibitorsMevalonic AcidMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Polyisoprenyl PhosphatesProto-Oncogene Proteins c-akt

Identifiers

PMID21831290
PMCPMC3163617
OpenAlexW2004021162

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.