Evidence map›Paper›PMID 25103771›Full record

ArticleJournal of cellular biochemistry2014

IL-1β induces p62/SQSTM1 and represses androgen receptor expression in prostate cancer cells.

M A Chang, V Patel, M Gwede, M Morgado, K Tomasevich, E L Fong, M C Farach-Carson, Nikki A Delk

Open access · greenAbstract read
In one paragraph

Article in Journal of cellular biochemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
0.7field-weighted citation impact, top 27% 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

30 citing papers in PubMed, 40 citations in OpenAlex.

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  12. Chronic IL-1 Exposed ARJournal of cellular signaling · 2021
    Article
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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

8 authors at 2 institutions in 1 country.

M A ChangDepartment of BioSciences, Rice University, BioScience Research Collaborative, 6500 Main, MS 601, Houston, TX, 77030.
V Patel
M Gwede
M Morgado
K Tomasevich
E L Fong
M C Farach-Carson
Nikki A Delk
Rice University · USThe University of Texas at Dallas · US

Funding

Prostate Cancer Bone Metastasis: Biology and TargetingP01CA098912 · NCI · EMORY UNIVERSITY · PI TIGHIOUART, MOURAD · 2003 to 2019
$24.0M
Cytoprotective Autophagy in Bone Metastatic Prostate CancerK01CA160602 · NCI · UNIVERSITY OF TEXAS DALLAS · PI DELK, NIKKI A · 2012 to 2016
$484k
Mechanistic regulation of tumor specific forms of cyclin E in breast cancerF32CA128296 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI DELK, NIKKI A · 2008 to 2010
$155k
NCI NIH HHS F32 CA128296NCI NIH HHS K01 CA160602NCI NIH HHS P01 CA098912
6 · The paper itself

Abstract

Chronic inflammation is associated with advanced prostate cancer (PCa), although the mechanisms governing inflammation-mediated PCa progression are not fully understood. PCa progresses to an androgen independent phenotype that is incurable. We previously showed that androgen independent, androgen receptor negative (AR(-) ) PCa cell lines have high p62/SQSTM1 levels required for cell survival. We also showed that factors in the HS-5 bone marrow stromal cell (BMSC) conditioned medium can upregulate p62 in AR(+) PCa cell lines, leading us to investigate AR expression under those growth conditions. In this paper, mRNA, protein, and subcellular analyses reveal that HS-5 BMSC conditioned medium represses AR mRNA, protein, and nuclear accumulation in the C4-2 PCa cell line. Using published gene expression data, we identify the inflammatory cytokine, IL-1β, as a candidate BMSC paracrine factor to regulate AR expression and find that IL-1β is sufficient to both repress AR and upregulate p62 in multiple PCa cell lines. Immunostaining demonstrates that, while the C4-2 population shows a primarily homogeneous response to factors in HS-5 BMSC conditioned medium, IL-1β elicits a strikingly heterogeneous response; suggesting that there are other regulatory factors in the conditioned medium. Finally, while we observe concomitant AR loss and p62 upregulation in IL-1β-treated C4-2 cells, silencing of AR or p62 suggests that IL-1β regulates their protein accumulation through independent pathways. Taken together, these in vitro results suggest that IL-1β can drive PCa progression in an inflammatory microenvironment through AR repression and p62 induction to promote the development and survival of androgen independent PCa.

Indexed as

Gene Expression Regulation, NeoplasticActive Transport, Cell NucleusAdaptor Proteins, Signal TransducingCell Line, TumorGene ExpressionHumansInterleukin-1betaMaleMesenchymal Stem CellsParacrine CommunicationProstatic NeoplasmsReceptors, AndrogenSequestosome-1 ProteinTranscriptional ActivationAdaptor Proteins, Signal TransducingInterleukin-1betaReceptors, AndrogenSequestosome-1 ProteinSQSTM1 protein, humanANDROGEN RECEPTORBONE MARROW STROMAL CELLSINFLAMMATIONINTERLEUKIN-1βp62/SEQUESTOME-1PROSTATE CANCER

Identifiers

PMID25103771
PMCPMC4517682
OpenAlexW1786063563

What OpenQuestion holds

Textmetadata
LicenceTDM
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.