Evidence map›Paper›PMID 25301738›Full record

ArticleOncotarget2014

Regulation of the viability of Nf1 deficient cells by PKC isoforms.

Xiaodong Zhou, Ling Shen, Toshima Parris, Junchi Huang, Bo Yi, Khalil Helou, Changyan Chen

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 35% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Review
  2. Article
  3. 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

7 authors at 4 institutions in 3 countries.

Xiaodong ZhouCenter for Drug Discovery, Northeastern University, Boston, USA. The First Affiliated Hospital of Nanchang University, Nanchang, China.
Ling ShenCenter for Drug Discovery, Northeastern University, Boston, USA.
Toshima ParrisThe Institute of Clinical Sciences, Gothenburg University, Gothenburg, SE.
Junchi HuangCenter for Drug Discovery, Northeastern University, Boston, USA.
Bo YiCenter for Drug Discovery, Northeastern University, Boston, USA. The Jiangxi Province Tumor Hospital, Nanchang, China.
Khalil HelouThe Institute of Clinical Sciences, Gothenburg University, Gothenburg, SE.
Changyan ChenCenter for Drug Discovery, Northeastern University, Boston, USA. The Institute of Clinical Sciences, Gothenburg University, Gothenburg, SE.
Northeastern University · USUniversity of Gothenburg · SEJiangxi Provincial Cancer Hospital · CNNanchang University · CN

Funding

Study of Anti-Survival signals in NF1R01CA153354 · NCI · NORTHEASTERN UNIVERSITY · PI CHEN, CHANGYAN · 2012 to 2017
$1.6M
NCI NIH HHS NIH R01CA153354NCI NIH HHS R01 CA153354
6 · The paper itself

Abstract

Suppression of protein kinase C (PKC) is known to be synthetically lethal with ras mutations in various types of cancer cells. The studies also showed that blockade of PKC affected the viability of Nf1 deficient cells. Since PKC family consists of more than 10 isoforms, our study aimed at identifying which isoform(s) played the crucial role in sensitizing Nf1 deficient cells to apoptosis. Using genetic and chemical PKC inhibitors, we demonstrated that the concurrent inhibition of PKC α and β induced Nf1 deficient ST or 96.2 cells, but not SNF02.2 cells with a normal Nf1 or ST cells ectopically expressing Nf1 effective domain gene, to apoptosis. In this process, PKC δ in Nf1 deficient cells, but not in ST/Nf1 cells, was upregulated and translocated to the nucleus. Furthermore, caspase 3 was cleaved and cytochrome c was released to the cytosol. Thus, it appeared that PKC δ and α/β are the crucial components for sustaining the aberrant Ras signaling and further viability of Nf1 deficient cells. The abrogation of these two isoforms activated their opponent PKC δ for switching on the caspase 3-governed apoptotic machinery.

Indexed as

ApoptosisCell ProliferationBlotting, WesternCaspasesCell CycleCells, CulturedCytochromes cHumansNeurofibromin 1Protein Kinase C-alphaProtein Kinase C betaProtein Kinase C-deltaProtein Kinase Inhibitorsras ProteinsReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionCaspasesCytochromes cNeurofibromin 1Protein Kinase C-alphaProtein Kinase C betaProtein Kinase C-deltaProtein Kinase Inhibitorsras ProteinsRNA, Messenger

Identifiers

PMID25301738
PMCPMC4279404
OpenAlexW1569109560

What OpenQuestion holds

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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.