Evidence map›Paper›PMID 17235455›Full record

ArticleMolecular and cellular biochemistry2007

PTEN down regulates AP-1 and targets c-fos in human glioma cells via PI3-kinase/Akt pathway.

Dimpy Koul, Ruijun Shen, Shishir Shishodia, Yasanuri Takada, Krishna P Bhat, Shrikanth A G Reddy, Bharat B Aggarwal, W K Alfred Yung

Abstract read
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In one paragraph

Article in Molecular and cellular biochemistry, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

18 citing papers in PubMed, 36 citations in OpenAlex.

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  8. CPEB4 interacts with Vimentin and involves in progressive features and poor prognosis of patients with astrocytic tumors.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
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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

8 authors at 1 institution in 1 country.

Dimpy KoulDepartment of Neuro-Oncology, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA. Dkoul@mdanderson.org
Ruijun Shen
Shishir Shishodia
Yasanuri Takada
Krishna P Bhat
Shrikanth A G Reddy
Bharat B Aggarwal
W K Alfred Yung
The University of Texas MD Anderson Cancer Center · US

Funding

DIFFERENTIALLY EXPRESSED GENE PRODUCTS IN HUMAN GLIOMASR01CA056041 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI YUNG, W K ALFRED · 1992 to 2007
$2.3M
NCI NIH HHS R01 CA 056041
6 · The paper itself

Abstract

The continual activation of signaling cascades results in dramatic consequences that include loss of cellular growth control and neoplastic transformation. We show here that phosphoinositide 3-kinase and its mediator Akt was constitutively activated in glioma and that this might be due to the aberrant expression of their natural antagonist PTEN. The PTEN (phosphatase and tensin homologue deleted on chromosome ten) tumor suppressor gene modulates cell growth and survival through mechanisms that are incompletely understood. In this study, we investigated the possibility that PTEN mediates its effects through modulation of transcription factor AP-1, which is in part due to decrease in c-fos expression which was dependent on PI3kinase activity. Consistent with a reduction in the c-fos levels, an AP-1 dependent reporter gene was poorly induced in the PTEN expressing cell lines. In contrast to its effect on c-fos, PTEN did not affect the expression of c-Jun and other fos family members. We also show that the effect of PTEN on c-fos expression was due to its ability to antagonize PI3-kinase and could be mimicked by the expression of dominant negative Akt mutant. Taken together, these data indicate that the aberrant expression of PTEN contributes to the activation of the PI3kinase/Akt pathway and its transcription factor mediators in glioma. We conclude that the ectopic expression of PTEN down regulates the proliferation of glioma cells through the suppression of AP-1 and that this target might be essential for its central role in the growth and survival of glioma cancer cells.

Indexed as

Down-RegulationCell Line, TumorEnzyme ActivationGene Expression Regulation, NeoplasticGenes, ReporterGliomaHumansPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-fosPTEN PhosphohydrolaseSignal TransductionTranscriptional ActivationTranscription Factor AP-1Tumor Necrosis Factor-alphaPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-fosPTEN PhosphohydrolasePTEN protein, humanTranscription Factor AP-1Tumor Necrosis Factor-alpha

Identifiers

PMID17235455
OpenAlexW2164158840

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.