Evidence map›Paper›PMID 23591848›Full record

ArticleInternational journal of molecular sciences2013

Loss of SUMOylation on ATF3 inhibits proliferation of prostate cancer cells by modulating CCND1/2 activity.

Chiung-Min Wang, Wei-Hsiung Yang

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.3field-weighted citation impact, top 37% 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

15 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. The dual role of ATF3 in myocardial repair through macrophage regulation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
  3. The impact of dysregulation SUMOylation on prostate cancer.Journal of translational medicine · 2025
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Forkhead Box Protein P3 (FOXP3) Represses ATF3 Transcriptional Activity.International journal of molecular sciences · 2021
    Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
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

2 authors at 1 institution in 1 country.

Chiung-Min WangDepartment of Biomedical Sciences, Mercer University School of Medicine, Savannah, GA 31404, USA. yang_w@mercer.edu.
Wei-Hsiung Yang
Mercer University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

SUMOylation plays an important role in regulating a wide range of cellular processes. Previously, we showed that ATF3, a stress response mediator, can be SUMOylated and lysine 42 is the major SUMO site. However, the significance of ATF3 SUMOylation in biological processes is still poorly understood. In the present study, we investigated the role of ATF3 SUMOylation on CCND activity and cellular proliferation in human prostate cancer cells. First, we showed that ATF3 can be SUMOylated endogenously in the overexpression system, and lysine 42 is the major SUMO site. Unlike normal prostate tissue and androgen-responsive LNCaP cancer cells, androgen-independent PC3 and DU145 cancer cells did not express ATF3 endogenously. Overexpression of ATF3 increased CCND1/2 expression in PC3 and DU145 cancer cells. Interestingly, we observed that SUMOylation is essential for ATF3-mediated CCND1/2 activation. Finally, we observed that SUMOylation plays a functional role in ATF3-mediated cellular proliferation in PC3 and DU145 cells. Taken together, our results demonstrate that SUMO modification of ATF3 influences CCND1/2 activity and cellular proliferation of prostate cancer PC3 and DU145 cells and explains at least in part how ATF3 functions to regulate cancer development.

Indexed as

Activating Transcription Factor 3Amino Acid SubstitutionAndrogensCell Line, TumorCell ProliferationCyclin D1Cyclin D2HumansLysineMaleMutagenesis, Site-DirectedNeoplasms, Hormone-DependentProstateProstatic NeoplasmsRecombinant ProteinsRNA, MessengerActivating Transcription Factor 3AndrogensATF3 protein, humanCCND1 protein, humanCCND2 protein, humanCyclin D1Cyclin D2LysineRecombinant ProteinsRNA, MessengerRNA, Neoplasm

Identifiers

PMID23591848
PMCPMC3645748
OpenAlexW2128681672

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.