Evidence map›Paper›PMID 25133482›Full record

ArticleOncogenesis2014

Lyn tyrosine kinase regulates androgen receptor expression and activity in castrate-resistant prostate cancer.

A Zardan, K M Nip, D Thaper, P Toren, S Vahid, E Beraldi, L Fazli, F Lamoureux, K M Gust, M E Cox and 2 more

Open access · goldAbstract read
In one paragraph

Article in Oncogenesis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
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

22 citing papers in PubMed, 29 citations in OpenAlex.

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  5. Fyn and Lyn gene polymorphisms impact the risk of thyroid cancer.Molecular genetics and genomics : MGG · 2022
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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

12 authors at 1 institution in 1 country.

A ZardanThe Vancouver Prostate Centre, University of British Columbia, Vancouver, British Columbia, Canada.
K M NipThe Vancouver Prostate Centre, University of British Columbia, Vancouver, British Columbia, Canada.
D ThaperThe Vancouver Prostate Centre, University of British Columbia, Vancouver, British Columbia, Canada.
P TorenThe Vancouver Prostate Centre, University of British Columbia, Vancouver, British Columbia, Canada.
S VahidThe Vancouver Prostate Centre, University of British Columbia, Vancouver, British Columbia, Canada.
E BeraldiThe Vancouver Prostate Centre, University of British Columbia, Vancouver, British Columbia, Canada.
L FazliThe Vancouver Prostate Centre, University of British Columbia, Vancouver, British Columbia, Canada.
F LamoureuxThe Vancouver Prostate Centre, University of British Columbia, Vancouver, British Columbia, Canada.
K M GustThe Vancouver Prostate Centre, University of British Columbia, Vancouver, British Columbia, Canada.
M E Cox1] The Vancouver Prostate Centre, University of British Columbia, Vancouver, British Columbia, Canada [2] Department of Urologic Sciences, University of British Columbia, Vancouver, British Columbia, Canada.
J L BishopThe Vancouver Prostate Centre, University of British Columbia, Vancouver, British Columbia, Canada.
A Zoubeidi1] The Vancouver Prostate Centre, University of British Columbia, Vancouver, British Columbia, Canada [2] Department of Urologic Sciences, University of British Columbia, Vancouver, British Columbia, Canada.
University of British Columbia · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Castrate-resistant prostate cancer (CRPC) progression is a complex process by which prostate cells acquire the ability to survive and proliferate in the absence or under very low levels of androgens. Most CRPC tumors continue to express the androgen receptor (AR) as well as androgen-responsive genes owing to reactivation of AR. Protein tyrosine kinases have been implicated in supporting AR activation under castrate conditions. Here we report that Lyn tyrosine kinase expression is upregulated in CRPC human specimens compared with hormone naive or normal tissue. Lyn overexpression enhanced AR transcriptional activity both in vitro and in vivo and accelerated CRPC. Reciprocally, specific targeting of Lyn resulted in a decrease of AR transcriptional activity in vitro and in vivo and prolonged time to castration. Mechanistically, we found that targeting Lyn kinase induces AR dissociation from the molecular chaperone Hsp90, leading to its ubiquitination and proteasomal degradation. This work indicates a novel mechanism of regulation of AR stability and transcriptional activity by Lyn and justifies further investigation of the Lyn tyrosine kinase as a therapeutic target for the treatment of CRPC.Oncogenesis (2014) 3, e115; doi:10.1038/oncsis.2014.30; published online 18 August 2014.

Identifiers

PMID25133482
PMCPMC5189960
OpenAlexW2027102691

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.