Evidence map›Paper›PMID 16103081›Full record

ArticleCancer research2005

Protein kinase C-epsilon regulates the apoptosis and survival of glioma cells.

Hana Okhrimenko, Wei Lu, Cunli Xiang, Nathan Hamburger, Gila Kazimirsky, Chaya Brodie

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 5% 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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 106 citations in OpenAlex.

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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

6 authors at 2 institutions in 2 countries.

Hana OkhrimenkoGonda (Goldschmied) Medical Diagnosis Research Center, Faculty of Life-Sciences, Bar-Ilan University, Ramat Gan, Israel.
Wei Lu
Cunli Xiang
Nathan Hamburger
Gila Kazimirsky
Chaya Brodie
Henry Ford Hospital · USBar-Ilan University · IL

Funding

Regulation of Glioma Cell Apoptosis in PKCDeltaR01CA109196 · NCI · HENRY FORD HEALTH SYSTEM · PI BRODIE, CHAYA · 2005 to 2008
$991k
NCI NIH HHS R01 CA109196NCI NIH HHS R01 CA109196-01A1
6 · The paper itself

Abstract

In this study, we examined the role of protein kinase C (PKC)-epsilon in the apoptosis and survival of glioma cells using tumor necrosis factor-related apoptosis inducing ligand (TRAIL)-stimulated cells and silencing of PKCepsilon expression. Treatment of glioma cells with TRAIL induced activation, caspase-dependent cleavage, and down-regulation of PKCepsilon within 3 to 5 hours of treatment. Overexpression of PKCepsilon inhibited the apoptosis induced by TRAIL, acting downstream of caspase 8 and upstream of Bid cleavage and cytochrome c release from the mitochondria. A caspase-resistant PKCepsilon mutant (D383A) was more protective than PKCepsilon, suggesting that both the cleavage of PKCepsilon and its down-regulation contributed to the apoptotic effect of TRAIL. To further study the role of PKCepsilon in glioma cell apoptosis, we employed short interfering RNAs directed against the mRNA of PKCepsilon and found that silencing of PKCepsilon expression induced apoptosis of various glioma cell lines and primary glioma cultures. To delineate the molecular mechanisms involved in the apoptosis induced by silencing of PKCepsilon, we examined the expression and phosphorylation of various apoptosis-related proteins. We found that knockdown of PKCepsilon did not affect the expression of Bcl2 and Bax or the phosphorylation and expression of Erk1/2, c-Jun-NH2-kinase, p38, or STAT, whereas it selectively reduced the expression of AKT. Similarly, TRAIL reduced the expression of AKT in glioma cells and this decrease was abolished in cells overexpressing PKCepsilon. Our results suggest that the cleavage of PKCepsilon and its down-regulation play important roles in the apoptotic effect of TRAIL. Moreover, PKCepsilon regulates AKT expression and is essential for the survival of glioma cells.

Indexed as

Amino Acid SequenceApoptosisApoptosis Regulatory ProteinsCaspasesCell Line, TumorDown-RegulationEnzyme ActivationGene SilencingGliomaHumansMembrane GlycoproteinsMolecular Sequence DataProtein Kinase CProtein Kinase C-epsilonProtein Serine-Threonine KinasesProto-Oncogene ProteinsAKT1 protein, humanApoptosis Regulatory ProteinsCaspasesMembrane GlycoproteinsPRKCE protein, humanProtein Kinase CProtein Kinase C-epsilonProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktRNA, MessengerRNA, Small InterferingTNF-Related Apoptosis-Inducing LigandTNFSF10 protein, humanTumor Necrosis Factor-alpha

Identifiers

PMID16103081
PMCPMC1360842
OpenAlexW2114632624

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.