Evidence map›Paper›PMID 25461807›Full record

ArticleBritish journal of cancer2015

BCAS2 promotes prostate cancer cells proliferation by enhancing AR mRNA transcription and protein stability.

P-C Kuo, C-W Huang, C-I Lee, H-W Chang, S-W Hsieh, Y-P Chung, M-S Lee, C-S Huang, L-P Tsao, Y-P Tsao and 1 more

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

13 citing papers in PubMed, 34 citations in OpenAlex.

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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

11 authors at 4 institutions in 1 country.

P-C KuoGraduate Institute of Microbiology, College of Medicine, National Taiwan University, Taipei 100, Taiwan.
C-W HuangGraduate Institute of Microbiology, College of Medicine, National Taiwan University, Taipei 100, Taiwan.
C-I LeeGraduate Institute of Microbiology, College of Medicine, National Taiwan University, Taipei 100, Taiwan.
H-W ChangGraduate Institute of Microbiology, College of Medicine, National Taiwan University, Taipei 100, Taiwan.
S-W HsiehTaipei Hospital, Ministry of Health and Welfare, New Taipei City 242, Taiwan.
Y-P ChungTaipei Hospital, Ministry of Health and Welfare, New Taipei City 242, Taiwan.
M-S LeeGraduate Institute of Biochemistry and Molecular Biology, College of Medicine, National Taiwan University, Taipei 100, Taiwan.
C-S HuangDepartment of Surgery, National Taiwan University Hospital, Taipei 100, Taiwani.
L-P TsaoGraduate Institute of Microbiology, College of Medicine, National Taiwan University, Taipei 100, Taiwan.
Y-P TsaoDepartment of Ophthalmology, Mackay Memorial Hospital, Taipei 104, Taiwan.
S-L ChenGraduate Institute of Microbiology, College of Medicine, National Taiwan University, Taipei 100, Taiwan.
National Taiwan University · TWMackay Memorial Hospital · TWMinistry of Health and Welfare · TWTaipei Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundWe showed previously that breast carcinoma amplified sequence 2 (BCAS2) functions as a negative regulator of p53. We also found that BCAS2 is a potential AR-associated protein. AR is essential for the growth and survival of prostate carcinoma. Therefore we characterised the correlation between BCAS2 and AR.

methodsProtein interactions were examined by GST pull-down assay and co-immunoprecipitation. Clinical prostate cancer (PCa) specimens were evaluated by immunohistochemical assay. AR transcriptional activity and LNCaP cell growth were assessed by luciferase assay and MTT assay, respectively.

resultsBCAS2 expression was significantly increased in PCa. BCAS2 stabilised AR protein through both hormone-dependent and -independent manners. There are at least two mechanisms for BCAS2-mediated AR protein upregulation: One is p53-dependent. The p53 is suppressed by BCAS2 that results in increasing AR mRNA and protein expression. The other is via p53-independent inhibition of proteasome degradation. As BCAS2 can form a complex with AR and HSP90, it may function with HSP90 to stabilise AR protein from being degraded by proteasome.

conclusionsIn this study, we show that BCAS2 is a novel AR-interacting protein and characterise the correlation between BCAS2 and PCa. Thus we propose that BCAS2 could be a diagnostic marker and therapeutic target for PCa.

Indexed as

Transcription, GeneticBenzoquinonesCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHalf-LifeHEK293 CellsHSP90 Heat-Shock ProteinsHumansInhibitory Concentration 50Lactams, MacrocyclicMaleNeoplasm GradingNeoplasm ProteinsProstatic NeoplasmsProteasome Endopeptidase ComplexBCAS2 protein, humanBenzoquinonesHSP90 Heat-Shock ProteinsLactams, MacrocyclicNeoplasm ProteinsProteasome Endopeptidase ComplexReceptors, AndrogentanespimycinTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID25461807
PMCPMC4453457
OpenAlexW2019741705

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.