Evidence map›Paper›PMID 25965834›Full record

ArticleOncotarget2015

CIP2A is a candidate therapeutic target in clinically challenging prostate cancer cell populations.

Anchit Khanna, Jayant K Rane, Kati K Kivinummi, Alfonso Urbanucci, Merja A Helenius, Teemu T Tolonen, Outi R Saramäki, Leena Latonen, Visa Manni, John E Pimanda and 3 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

14 citing papers in PubMed, 28 citations in OpenAlex.

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

13 authors at 6 institutions in 4 countries.

Anchit KhannaProstate Cancer Research Center (PCRC), Institute of Biosciences and Medical Technology (BioMediTech), University of Tampere and Tampere University Hospital, Tampere, Finland.
Jayant K RaneYCR Cancer Research Unit, Department of Biology, The University of York, Heslington, United Kingdom.
Kati K KivinummiProstate Cancer Research Center (PCRC), Institute of Biosciences and Medical Technology (BioMediTech), University of Tampere and Tampere University Hospital, Tampere, Finland.
Alfonso UrbanucciProstate Cancer Research Center (PCRC), Institute of Biosciences and Medical Technology (BioMediTech), University of Tampere and Tampere University Hospital, Tampere, Finland.
Merja A HeleniusProstate Cancer Research Center (PCRC), Institute of Biosciences and Medical Technology (BioMediTech), University of Tampere and Tampere University Hospital, Tampere, Finland.
Teemu T TolonenProstate Cancer Research Center (PCRC), Institute of Biosciences and Medical Technology (BioMediTech), University of Tampere and Tampere University Hospital, Tampere, Finland.
Outi R SaramäkiProstate Cancer Research Center (PCRC), Institute of Biosciences and Medical Technology (BioMediTech), University of Tampere and Tampere University Hospital, Tampere, Finland.
Leena LatonenProstate Cancer Research Center (PCRC), Institute of Biosciences and Medical Technology (BioMediTech), University of Tampere and Tampere University Hospital, Tampere, Finland.
Visa ManniProstate Cancer Research Center (PCRC), Institute of Biosciences and Medical Technology (BioMediTech), University of Tampere and Tampere University Hospital, Tampere, Finland.
John E PimandaAdult Cancer Program, The Prince of Wales Clinical School, Lowy Cancer Research Centre, UNSW Medicine, University of New South Wales, Sydney, Australia.
Norman J MaitlandYCR Cancer Research Unit, Department of Biology, The University of York, Heslington, United Kingdom.
Jukka WestermarckTurku Centre for Biotechnology, University of Turku and Åbo Akademi University, Turku, Finland.
Tapio VisakorpiProstate Cancer Research Center (PCRC), Institute of Biosciences and Medical Technology (BioMediTech), University of Tampere and Tampere University Hospital, Tampere, Finland.
Tampere University Hospital · FITampere University · FIUniversity of Turku · FIUniversity of York · GBUNSW Sydney · AUYorkshire Cancer Research · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Residual androgen receptor (AR)-signaling and presence of cancer stem-like cells (SCs) are the two emerging paradigms for clinically challenging castration-resistant prostate cancer (CRPC). Therefore, identification of AR-target proteins that are also overexpressed in the cancer SC population would be an attractive therapeutic approach.Our analysis of over three hundred clinical samples and patient-derived prostate epithelial cultures (PPECs), revealed Cancerous inhibitor of protein phosphatase 2A (CIP2A) as one such target. CIP2A is significantly overexpressed in both hormone-naïve prostate cancer (HN-PC) and CRPC patients . CIP2A is also overexpressed, by 3- and 30-fold, in HN-PC and CRPC SCs respectively. In vivo binding of the AR to the intronic region of CIP2A and its functionality in the AR-moderate and AR-high expressing LNCaP cell-model systems is also demonstrated. Further, we show that AR positively regulates CIP2A expression, both at the mRNA and protein level. Finally, CIP2A depletion reduced cell viability and colony forming efficiency of AR-independent PPECs as well as AR-responsive LNCaP cells, in which anchorage-independent growth is also impaired.These findings identify CIP2A as a common denominator for AR-signaling and cancer SC functionality, highlighting its potential therapeutic significance in the most clinically challenging prostate pathology: castration-resistant prostate cancer.

Indexed as

Androgen AntagonistsAntineoplastic Agents, HormonalAutoantigensBinding SitesCell Line, TumorCell ProliferationCell SurvivalGene Expression Regulation, NeoplasticGenetic TherapyHumansIntracellular Signaling Peptides and ProteinsIntronsMaleMembrane ProteinsMolecular Targeted TherapyNeoplastic Stem CellsAndrogen AntagonistsAntineoplastic Agents, HormonalAR protein, humanAutoantigensCIP2A protein, humanIntracellular Signaling Peptides and ProteinsMembrane ProteinsReceptors, AndrogenRNA, Messengerandrogen receptorcancer stem-like cellscastration-resistant prostate cancerCIP2A

Identifiers

PMID25965834
PMCPMC4637312
OpenAlexW2163819788

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.