Evidence map›Paper›PMID 25531328›Full record

ArticleOncogene2015

Loss of ATF3 promotes Akt activation and prostate cancer development in a Pten knockout mouse model.

Z Wang, D Xu, H-F Ding, J Kim, J Zhang, T Hai, C Yan

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

50 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
  2. Article
  3. JUNB and JUND in Urological Cancers: A Literature Review.Current issues in molecular biology · 2025
    Review
  4. Mechanism of Ferroptosis and Its Role in Disease Development.International journal of biological sciences · 2025
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. ATF3 in atherosclerosis: a controversial transcription factor.Journal of molecular medicine (Berlin, Germany) · 2022
    Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

7 authors at 4 institutions in 1 country.

Z WangGRU Cancer Center, Georgia Regents University, Augusta, GA, USA.
D XuCenter for Cell Biology and Cancer Research, Albany Medical College, Albany, NY, USA.
H-F DingGRU Cancer Center, Georgia Regents University, Augusta, GA, USA.
J KimDepartment of Biostatistics & Epidemiology, Georgia Regents University, Augusta, GA, USA.
J ZhangDepartment of Radiation Oncology, School of Medicine, Case Western Reserve University, Cleveland, OH, USA.
T HaiDepartment of Molecular and Cellular Biochemistry, Ohio State University, Columbus, OH, USA.
C YanGRU Cancer Center, Georgia Regents University, Augusta, GA, USA.
Augusta University · USAlbany Medical Center Hospital · USCase Western Reserve University · USThe Ohio State University · US

Funding

THE ROLE OF NEDD4-1 IN IGF-1R SIGNALINGR01CA154625 · NCI · WASHINGTON UNIVERSITY · PI ZHANG, JUNRAN · 2011 to 2016
$1.6M
The Role of ATF3 in the DNA Damage ResponseR01CA139107 · NCI · AUGUSTA UNIVERSITY · PI YAN, CHUNHONG · 2010 to 2015
$1.2M
Screening Assays for Small Molecules Targeting Oncogenic eIF4E ExpressionR01CA164006 · NCI · AUGUSTA UNIVERSITY · PI YAN, CHUNHONG · 2012 to 2014
$832k
NCI NIH HHS R01 CA139107NCI NIH HHS R01CA139107NCI NIH HHS R01 CA154625NCI NIH HHS R01 CA164006NCI NIH HHS R01CA164006
6 · The paper itself

Abstract

Activating transcription factor 3 (ATF3) responds to diverse cellular stresses, and regulates oncogenic activities (for example, proliferation, survival and migration) through direct transcriptional regulation or protein-protein interactions. Although aberrant ATF3 expression is frequently found in human cancers, the role of ATF3 in tumorigenesis is poorly understood. Here, we demonstrate that ATF3 suppresses the development of prostate cancer induced by knockout of the tumor suppressor Pten in mouse prostates. Whereas the oncogenic stress elicited by Pten loss induced ATF3 expression in prostate epithelium, we found that ATF3 deficiency increased cell proliferation and promoted cell survival, leading to early onset of mouse prostatic intraepithelial neoplasia and the progression of prostate lesions to invasive adenocarcinoma. Importantly, the loss of ATF3 promoted activation of the oncogenic AKT signaling evidenced by high levels of phosphorylated AKT and S6 proteins in ATF3-null prostate lesions. In line with these in vivo results, knockdown of ATF3 expression in human prostate cancer cells by single guided RNA-mediated targeting activated AKT and increased matrix metalloproteinase-9 expression. Our results thus link ATF3 to the AKT signaling, and suggest that ATF3 is a tumor suppressor for the major subset of prostate cancers harboring dysfunctional Pten.

Indexed as

Activating Transcription Factor 3AnimalsCell Line, TumorDisease Models, AnimalEnzyme ActivationMaleMatrix Metalloproteinase 2Matrix Metalloproteinase 9MiceMice, Inbred C57BLMice, KnockoutNF-kappa BProstatic NeoplasmsProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseSignal TransductionActivating Transcription Factor 3Atf3 protein, mouseMatrix Metalloproteinase 2Matrix Metalloproteinase 9NF-kappa BProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePten protein, mouse

Identifiers

PMID25531328
PMCPMC4476969
OpenAlexW2070697701

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.