Evidence map›Paper›PMID 26023836›Full record

ArticleMarine drugs2015

Activation of the Tumor Suppressor PP2A Emerges as a Potential Therapeutic Strategy for Treating Prostate Cancer.

Ion Cristóbal, Paula González-Alonso, Lina Daoud, Esther Solano, Blanca Torrejón, Rebeca Manso, Juan Madoz-Gúrpide, Federico Rojo, Jesús García-Foncillas

Open access · goldAbstract read
In one paragraph

Article in Marine drugs, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed, 30 citations in OpenAlex.

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  14. Synergistic Interaction ofClinical cancer research : an official journal of the American Association for Cancer Research · 2018
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  19. 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
  20. Review
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

9 authors at 1 institution in 1 country.

Ion CristóbalTranslational Oncology Division, Oncohealth Institute, IIS-Fundacion Jimenez Diaz, UAM, University Hospital "Fundacion Jimenez Diaz", E-28040 Madrid, Spain. ion.cristobal@fjd.es.
Paula González-AlonsoGroup of Cancer Biomarkers, Pathology Department, IIS-Fundacion Jimenez Diaz, UAM, E-28040 Madrid, Spain.
Lina DaoudGroup of Cancer Biomarkers, Pathology Department, IIS-Fundacion Jimenez Diaz, UAM, E-28040 Madrid, Spain. daoudlina@gmail.com.
Esther SolanoGroup of Cancer Biomarkers, Pathology Department, IIS-Fundacion Jimenez Diaz, UAM, E-28040 Madrid, Spain. esthersbasket4@gmail.com.
Blanca TorrejónTranslational Oncology Division, Oncohealth Institute, IIS-Fundacion Jimenez Diaz, UAM, University Hospital "Fundacion Jimenez Diaz", E-28040 Madrid, Spain. blanca.torrejonmoreno@gmail.com.
Rebeca MansoGroup of Cancer Biomarkers, Pathology Department, IIS-Fundacion Jimenez Diaz, UAM, E-28040 Madrid, Spain. rebeca.manso@fjd.es.
Juan Madoz-GúrpideGroup of Cancer Biomarkers, Pathology Department, IIS-Fundacion Jimenez Diaz, UAM, E-28040 Madrid, Spain. jmadoz@fjd.es.
Federico RojoGroup of Cancer Biomarkers, Pathology Department, IIS-Fundacion Jimenez Diaz, UAM, E-28040 Madrid, Spain. frojo@fjd.es.
Jesús García-FoncillasTranslational Oncology Division, Oncohealth Institute, IIS-Fundacion Jimenez Diaz, UAM, University Hospital "Fundacion Jimenez Diaz", E-28040 Madrid, Spain. blanca.torrejonmoreno@gmail.com.
Hospital Universitario Fundación Jiménez Díaz · ES

Funding

NIMHD NIH HHS L60 MD002344
6 · The paper itself

Abstract

Protein phosphatase 2A (PP2A) is a tumor suppressor complex that has recently been reported as a novel and highly relevant molecular target in prostate cancer (PCa). However, its potential therapeutic value remains to be fully clarified. We treated PC-3 and LNCaP cell lines with the PP2A activators forskolin and FTY720 alone or combined with the PP2A inhibitor okadaic acid. We examined PP2A activity, cell growth, prostasphere formation, levels of PP2A phosphorylation, CIP2A and SET expression, and AKT and ERK activation. Interestingly, both forskolin and FTY720 dephosphorylated and activated PP2A, impairing proliferation and prostasphere formation and inducing changes in AKT and ERK phosphorylation. Moreover, FTY720 led to reduced CIP2A levels. Treatment with okadaic acid impaired PP2A activation thus demonstrating the antitumoral PP2A-dependent mechanism of action of both forskolin and FTY720. Levels of PP2A phosphorylation together with SET and CIP2A protein expression were studied in 24 PCa patients and both were associated with high Gleason scores and presence of metastatic disease. Altogether, our results suggest that PP2A inhibition could be involved in PCa progression, and the use of PP2A-activating drugs might represent a novel alternative therapeutic strategy for treating PCa patients.

Indexed as

Molecular Targeted TherapyAntineoplastic AgentsCell Line, TumorCell ProliferationColforsinFingolimod HydrochlorideHumansMaleOkadaic AcidPhosphorylationProstatic NeoplasmsProtein Phosphatase 2Antineoplastic AgentsColforsinFingolimod HydrochlorideOkadaic AcidProtein Phosphatase 2CIP2Aokadaic acidp-PP2Aprostate cancertherapy

Identifiers

PMID26023836
PMCPMC4483628
OpenAlexW1571338740

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.