Evidence map›Paper›PMID 25552417›Full record

ArticleNucleic acids research2015

SUMO ligase PIAS1 functions as a target gene selective androgen receptor coregulator on prostate cancer cell chromatin.

Sari Toropainen, Marjo Malinen, Sanna Kaikkonen, Miia Rytinki, Tiina Jääskeläinen, Biswajyoti Sahu, Olli A Jänne, Jorma J Palvimo

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2015. 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
5.6field-weighted citation impact, top 4% 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, 70 citations in OpenAlex.

  1. Pooled it
  2. Regulation of lineage reprogramming by dynamic chromatin SUMOylation.Cellular and molecular life sciences : CMLS · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. The impact of dysregulation SUMOylation on prostate cancer.Journal of translational medicine · 2025
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. 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.

Sari ToropainenInstitute of Biomedicine, University of Eastern Finland, FI-70211 Kuopio, Finland.
Marjo MalinenInstitute of Biomedicine, University of Eastern Finland, FI-70211 Kuopio, Finland.
Sanna KaikkonenInstitute of Biomedicine, University of Eastern Finland, FI-70211 Kuopio, Finland.
Miia RytinkiInstitute of Biomedicine, University of Eastern Finland, FI-70211 Kuopio, Finland.
Tiina JääskeläinenInstitute of Biomedicine, University of Eastern Finland, FI-70211 Kuopio, Finland Institute of Dentistry, University of Eastern Finland, FI-70211 Kuopio, Finland.
Biswajyoti SahuInstitute of Biomedicine, Physiology, Biomedicum Helsinki, University of Helsinki, FI-00014 Helsinki, Finland Research Programs Unit, Genome-Scale Biology, Biomedicum Helsinki, University of Helsinki, FI-00014 Helsinki, Finland.
Olli A JänneInstitute of Biomedicine, Physiology, Biomedicum Helsinki, University of Helsinki, FI-00014 Helsinki, Finland.
Jorma J PalvimoInstitute of Biomedicine, University of Eastern Finland, FI-70211 Kuopio, Finland jorma.palvimo@uef.fi.
University of Eastern Finland · FIUniversity of Helsinki · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Androgen receptor (AR) is a ligand-activated transcription factor that plays a central role in the development and growth of prostate carcinoma. PIAS1 is an AR- and SUMO-interacting protein and a putative transcriptional coregulator overexpressed in prostate cancer. To study the importance of PIAS1 for the androgen-regulated transcriptome of VCaP prostate cancer cells, we silenced its expression by RNAi. Transcriptome analyses revealed that a subset of the AR-regulated genes is significantly influenced, either activated or repressed, by PIAS1 depletion. Interestingly, PIAS1 depletion also exposed a new set of genes to androgen regulation, suggesting that PIAS1 can mask distinct genomic loci from AR access. In keeping with gene expression data, silencing of PIAS1 attenuated VCaP cell proliferation. ChIP-seq analyses showed that PIAS1 interacts with AR at chromatin sites harboring also SUMO2/3 and surrounded by H3K4me2; androgen exposure increased the number of PIAS1-occupying sites, resulting in nearly complete overlap with AR chromatin binding events. PIAS1 interacted also with the pioneer factor FOXA1. Of note, PIAS1 depletion affected AR chromatin occupancy at binding sites enriched for HOXD13 and GATA motifs. Taken together, PIAS1 is a genuine chromatin-bound AR coregulator that functions in a target gene selective fashion to regulate prostate cancer cell growth.

Indexed as

Gene Expression Regulation, NeoplasticBinding SitesCell Line, TumorCell ProliferationChromatinHepatocyte Nuclear Factor 3-alphaHumansMaleProstatic NeoplasmsProtein Inhibitors of Activated STATReceptors, AndrogenSmall Ubiquitin-Related Modifier ProteinsUbiquitin-Protein LigasesChromatinFOXA1 protein, humanHepatocyte Nuclear Factor 3-alphaPIAS1 protein, humanProtein Inhibitors of Activated STATReceptors, AndrogenSmall Ubiquitin-Related Modifier ProteinsUbiquitin-Protein Ligases

Identifiers

PMID25552417
PMCPMC4333416
OpenAlexW2007054651

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.