Evidence map›Paper›PMID 17189429›Full record

ArticleMolecular and cellular biology2007

Reduced levels of ATF-2 predispose mice to mammary tumors.

Toshio Maekawa, Toshie Shinagawa, Yuji Sano, Takahiko Sakuma, Shintaro Nomura, Koichi Nagasaki, Yoshio Miki, Fumiko Saito-Ohara, Johji Inazawa, Takashi Kohno and 2 more

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Molecular and cellular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
2.3field-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

46 citing papers in PubMed, 82 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. SPOP promotes ATF2 ubiquitination and degradation to suppress prostate cancer progression.Journal of experimental & clinical cancer research : CR · 2018
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. miRNA-204 suppresses human non-small cell lung cancer by targeting ATF2.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  11. ATF2 predicts poor prognosis and promotes malignant phenotypes in renal cell carcinoma.Journal of experimental & clinical cancer research : CR · 2016
    Article
  12. Genetic variants in EBV reactivation-related genes and the risk and survival of breast cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Inhibition of melanoma growth by small molecules that promote the mitochondrial localization of ATF2.Clinical cancer research : an official journal of the American Association for Cancer Research · 2013
    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

12 authors at 5 institutions in 3 countries.

Toshio MaekawaLaboratory of Molecular Genetics, RIKEN Tsukuba Institute, 3-1-1 Koyadai, Tsukuba, Ibaraki 305-0074, Japan.
Toshie Shinagawa
Yuji Sano
Takahiko Sakuma
Shintaro Nomura
Koichi Nagasaki
Yoshio Miki
Fumiko Saito-Ohara
Johji Inazawa
Takashi Kohno
Jun Yokota
Shunsuke Ishii
Laboratory of Molecular Genetics · PLJapanese Foundation For Cancer Research · JPNational Cancer Research Institute · GBThe University of Osaka · JPTokyo Medical and Dental University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transcription factor ATF-2 is a nuclear target of stress-activated protein kinases, such as p38, which are activated by various extracellular stresses, including UV light. Here, we show that ATF-2 plays a critical role in hypoxia- and high-cell-density-induced apoptosis and the development of mammary tumors. Compared to wild-type cells, Atf-2(-/-) mouse embryonic fibroblasts (MEFs) were more resistant to hypoxia- and anisomycin-induced apoptosis but remained equally susceptible to other stresses, including UV. Atf-2(-/-) and Atf-2(+/-) MEFs could not express a group of genes, such as Gadd45alpha, whose overexpression can induce apoptosis, in response to hypoxia. Atf-2(-/-) MEFs also had a higher saturation density than wild-type cells and expressed lower levels of Maspin, the breast cancer tumor suppressor, which is also known to enhance cellular sensitivity to apoptotic stimuli. Atf-2(-/-) MEFs underwent a lower degree of apoptosis at high cell density than wild-type cells. Atf-2(+/-) mice were highly prone to mammary tumors that expressed reduced levels of Gadd45alpha and Maspin. The ATF-2 mRNA levels in human breast cancers were lower than those in normal breast tissue. Thus, ATF-2 acts as a tumor susceptibility gene of mammary tumors, at least partly, by activating a group of target genes, including Maspin and Gadd45alpha.

Indexed as

Genetic Predisposition to DiseaseActivating Transcription Factor 2AnimalsAnisomycinApoptosisBreast NeoplasmsCell Cycle ProteinsCell HypoxiaFemaleFibroblastsGADD45 ProteinsGenes, ReporterGenes, Tumor SuppressorHumansMammary Neoplasms, AnimalMiceActivating Transcription Factor 2AnisomycinAtf2 protein, mouseCell Cycle ProteinsGadd45a protein, mouseGADD45 ProteinsNuclear ProteinsNucleic Acid Synthesis InhibitorsRNA, MessengerSERPIN-B5Serpins

Identifiers

PMID17189429
PMCPMC1820478
OpenAlexW2127071077

What OpenQuestion holds

Textmetadata
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.