Evidence map›Paper›PMID 29269934›Full record

ArticleScientific reports2017

The expression of AURKA is androgen regulated in castration-resistant prostate cancer.

Kati Kivinummi, Alfonso Urbanucci, Katri Leinonen, Teuvo L J Tammela, Matti Annala, William B Isaacs, G Steven Bova, Matti Nykter, Tapio Visakorpi

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 9% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.

  1. Pooled it
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  11. Selective Aurora A-TPX2 Interaction Inhibitors HaveJournal of medicinal chemistry · 2024
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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

9 authors at 4 institutions in 3 countries.

Kati KivinummiBioMediTech Institute, Faculty of Medicine and Life Sciences, University of Tampere, Fimlab Laboratories, Tampere University Hospital, Tampere, Finland. kati.kivinummi@uta.fi.ORCID 0000-0002-5788-835X
Alfonso UrbanucciBioMediTech Institute, Faculty of Medicine and Life Sciences, University of Tampere, Fimlab Laboratories, Tampere University Hospital, Tampere, Finland.
Katri LeinonenBioMediTech Institute, Faculty of Medicine and Life Sciences, University of Tampere, Fimlab Laboratories, Tampere University Hospital, Tampere, Finland.
Teuvo L J TammelaDepartment of Urology, Tampere University Hospital and Faculty of Medicine and Life Sciences, University of Tampere, Tampere, Finland.
Matti AnnalaBioMediTech Institute, Faculty of Medicine and Life Sciences, University of Tampere, Fimlab Laboratories, Tampere University Hospital, Tampere, Finland.
William B IsaacsThe James Buchanan Brady Urological Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland, 21287, USA.
G Steven BovaBioMediTech Institute, Faculty of Medicine and Life Sciences, University of Tampere, Fimlab Laboratories, Tampere University Hospital, Tampere, Finland.
Matti NykterBioMediTech Institute, Faculty of Medicine and Life Sciences, University of Tampere, Fimlab Laboratories, Tampere University Hospital, Tampere, Finland.
Tapio VisakorpiBioMediTech Institute, Faculty of Medicine and Life Sciences, University of Tampere, Fimlab Laboratories, Tampere University Hospital, Tampere, Finland.
Tampere University · FIJohns Hopkins University · USOslo University Hospital · NOTampere University Hospital · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although second generation endocrine therapies have significantly improved survival, castration-resistant prostate cancer (CRPC) cells are eventually able to escape available hormonal treatments due to reactivation of androgen receptor (AR) signaling. Identification of novel, non-classical and druggable AR-target genes may provide new approaches to treat CRPC. Our previous analyses suggested that Aurora kinase A (AURKA) is regulated by androgens in prostate cancer cells that express high levels of AR. Here, we provide further evidence that AURKA is significantly overexpressed in AR-positive CRPC samples carrying amplification of AR gene and/or expressing AR in high levels. We also demonstrate androgen-induced AR binding in the intronic region of AURKA. The expression of AURKA is increased upon androgen stimulation in LNCaP-ARhi cells that express high levels of AR. The growth of the cells was also significantly inhibited by an AURKA specific inhibitor, alisertib (MLN8237). Together, these findings suggest that the expression of AURKA is regulated by androgen in prostate cancer cells that highly express AR, emphasizing its potential as a therapeutic target in patients with CRPC.

Indexed as

AndrogensAurora Kinase AHumansMalePolymerase Chain ReactionProstatic Neoplasms, Castration-ResistantReceptors, AndrogenAndrogensAURKA protein, humanAurora Kinase AReceptors, Androgen

Identifiers

PMID29269934
PMCPMC5740165
OpenAlexW2772229485

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.