Evidence map›Paper›PMID 29594945›Full record

ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2018

Nur77 suppression facilitates androgen deprivation-induced cell invasion of prostate cancer cells mediated by TGF-β signaling.

J Wu, H Sun, X Yang, X Sun

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In one paragraph

Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.2field-weighted citation impact, top 54% 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

4 citing papers in PubMed, 5 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

4 authors at 3 institutions in 2 countries.

J WuDepartment of Urology, Drum Tower Hospital, Medical School of Nanjing University, 321 Zhongshan Rd, Nanjing, 210008, Jiangsu, China.
H SunDepartment of Urology, Nanjing First Hospital, Nanjing Medical University, Nanjing, 210000, Jiangsu, China.
X YangInstitute of Business Analytics, University of Alabama, Tuscaloosa, AL, 35401, USA.
X SunDepartment of Urology, Drum Tower Hospital, Medical School of Nanjing University, 321 Zhongshan Rd, Nanjing, 210008, Jiangsu, China. sunxzh1892@126.com.ORCID http://orcid.org/0000-0003-3037-7901
Nanjing Drum Tower Hospital · CNNanjing Medical University · CNUniversity of Alabama · US

Funding

Nanjing Medical Science and Technology Development Program ykk15904
6 · The paper itself

Abstract

backgroundAndrogen deprivation therapy (ADT) remains a standard treatment for advanced prostate cancers. However, recent studies revealed that while inhibiting the growth of certain types of prostate cancer cells, ADT promotes invasion. In the current study, we explored the effects of Nur77, an orphan nuclear receptor, on prostate cancer cell invasion following ADT.

methodsAndrogen receptor (AR) and Nur77 protein expression in patient tissues and cell lines were quantified via ELISA and western blot. The effects of AR-signaling on Nur77 expression were examined. The effects of Nur77 over-expression and knockdown on ADT-induced prostate cancer cell invasion were characterized.

resultsThe results showed that AR and Nur77 are both highly expressed in prostate cancers of patients. Nur77 is positively regulated by AR-signaling at transcriptional level in NCI-H660, a widely used prostate cancer cell line. AR antagonists, Casodex and MDV3100 treatment resulted in significant inhibition of prostate cancer cell growth but enhanced cancer cell invasion. Nur77 over-expression blocked invasion-promoting effect of ADT, which is consistent with the down-regulation of MMP9 and Snail protein expression. Further mechanistic investigations showed that Nur77 inhibited transcription of TGF-β target genes (Snail and MMP9), and thereby inhibits TGF-β-mediated prostate cancer cell invasion following androgen antagonism. In addition, our data suggested the nature of this inhibitory effect of Nur77 on TGF-β-signaling is selective, for Smad3-signaling, the classical effector of TGF-β-signaling, was not interrupted by Nur77 over-expression.

conclusionConsidering the limited success of management of prostate cancer metastasis following ADT, our data strongly suggest that Nur77 regulation could be a promising direction for search of complementary therapeutic strategy on top of classic ADT therapy.

Indexed as

Androgen AntagonistsGene Expression Regulation, NeoplasticHumansMaleNeoplasm InvasivenessNuclear Receptor Subfamily 4, Group A, Member 1Prostatic NeoplasmsReceptors, AndrogenSignal TransductionTransforming Growth Factor betaAndrogen AntagonistsAR protein, humanNR4A1 protein, humanNuclear Receptor Subfamily 4, Group A, Member 1Receptors, AndrogenTransforming Growth Factor betaAndrogen deprivationAndrogen receptorCancer cell invasionNur77Prostate cancer

Identifiers

PMID29594945
OpenAlexW2794755794

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Registered trials

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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.