Evidence map›Paper›PMID 23598299›Full record

ArticleBritish journal of cancer2013

Impaired expression of protein phosphatase 2A subunits enhances metastatic potential of human prostate cancer cells through activation of AKT pathway.

P Pandey, P Seshacharyulu, S Das, S Rachagani, M P Ponnusamy, Y Yan, S L Johansson, K Datta, M Fong Lin, S K Batra

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

25 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. PP2A is activated by cytochromeComputational and structural biotechnology journal · 2022
    Article
  5. Review
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  20. PP2A inhibition as a novel therapeutic target in castration-resistant prostate cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    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

10 authors at 1 institution in 1 country.

P PandeyDepartment of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE 68198-5870, USA.
P Seshacharyulu
S Das
S Rachagani
M P Ponnusamy
Y Yan
S L Johansson
K Datta
M Fong Lin
S K Batra
University of Nebraska Medical Center · US

Funding

Novel deregulated genes in the etiology and progression of human prostate cancerR01CA138791 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BATRA, SURINDER K. · 2010 to 2014
$1.9M
The role of VEGF-C in resisting stress in prostate cancerR01CA140432 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI DATTA, KAUSTUBH · 2010 to 2014
$1.5M
NCI NIH HHS R01 CA138791NCI NIH HHS R01 CA140432
6 · The paper itself

Abstract

backgroundProtein phosphatase 2A (PP2A) is a dephosphorylating enzyme, loss of which can contribute to prostate cancer (PCa) pathogenesis. The aim of this study was to analyse the transcriptional and translational expression patterns of individual subunits of the PP2A holoenzyme during PCa progression.

methodsImmunohistochemistry (IHC), western blot, and real-time PCR was performed on androgen-dependent (AD) and androgen-independent (AI) PCa cells, and benign and malignant prostate tissues for all the three PP2A (scaffold, regulatory, and catalytic) subunits. Mechanistic and functional studies were performed using various biochemical and cellular techniques.

resultsThrough immunohistochemical analysis we observed significantly reduced levels of PP2A-A and -B'γ subunits (P<0.001 and P=0.0002) in PCa specimens compared with benign prostate. Contemporarily, there was no significant difference in PP2A-C subunit expression between benign and malignant tissues. Similar to the expression pattern observed in tissues, the endogenous levels of PP2A-A and B'γ subunits were abrogated from the low metastatic to high metastatic and AD to AI cell line models, without any change in the catalytic subunit expression. Furthermore, using in vitro studies we demonstrated that PP2A-Aα scaffold subunit has a role in dampening AKT, β-catenin, and FAK (focal adhesion kinase) signalling.

conclusionWe conclude that loss of expression of scaffold and regulatory subunits of PP2A is responsible for its altered function during PCa pathogenesis.

Indexed as

AdenocarcinomaCell Line, TumorDisease ProgressionDown-RegulationEnzyme ActivationGene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticHumansMaleModels, BiologicalNeoplasm MetastasisOncogene Protein v-aktProstatic NeoplasmsProtein Phosphatase 2Protein SubunitsSignal TransductionOncogene Protein v-aktPPP2CA protein, humanProtein Phosphatase 2Protein Subunits

Identifiers

PMID23598299
PMCPMC3694226
OpenAlexW2071809116

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.