Evidence map›Paper›PMID 20066163›Full record

ArticleJournal of oncology2009

AP-2alpha Inhibits c-MYC Induced Oxidative Stress and Apoptosis in HaCaT Human Keratinocytes.

Lei Yu, Michael J Hitchler, Wenqing Sun, Ehab H Sarsour, Prabhat C Goswami, Aloysius J Klingelhutz, Frederick E Domann

Open access · hybridAbstract read
In one paragraph

Article in Journal of oncology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

16 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Methyltransferase Set7/9 as a Multifaceted Regulator of ROS Response.International journal of biological sciences · 2023
    Review
  5. Isotretinoin and Thalidomide Down-RegulateMolecules (Basel, Switzerland) · 2021
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Ectopic expression of AP-2α transcription factor suppresses glioma progression.International journal of clinical and experimental pathology · 2014
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. 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 1 institution in 1 country.

Lei YuFree Radical & Radiation Biology Graduate Program, Radiation Oncology Department, Roy J. and Lucille A. Carver College of Medicine, The University of Iowa, Iowa City, IA 52242, USA.
Michael J Hitchler
Wenqing Sun
Ehab H Sarsour
Prabhat C Goswami
Aloysius J Klingelhutz
Frederick E Domann
University of Iowa · US

Funding

Viral VectorP30CA086862 · NCI · UNIVERSITY OF IOWA · PI Douglas Robert Spitz · 2000 to 2026
$70.0M
Redox Biology of Quiescent Normal Fibroblasts and Epithelial Cancer ProgressionR01CA111365 · NCI · UNIVERSITY OF IOWA · PI GOSWAMI, PRABHAT C · 2006 to 2016
$2.1M
A Human Model for Telomerase Dysfunction and AgingR01AG027388 · NIA · UNIVERSITY OF IOWA · PI KLINGELHUTZ, ALOYSIUS JOHN · 2007 to 2011
$1.3M
Epigenetic factors governing SOD2 gene expressionR01CA073612 · NCI · UNIVERSITY OF IOWA · PI DOMANN, FREDERICK E · 2003 to 2007
$1.3M
Molecular Species Responsible for Tumor Supressive Effect of MnSODR01CA115438 · NCI · UNIVERSITY OF IOWA · PI DOMANN, FREDERICK E · 2007 to 2011
$1.2M
NCI NIH HHS P30 CA086862NCI NIH HHS R01 CA073612NCI NIH HHS R01 CA111365NCI NIH HHS R01 CA115438NIA NIH HHS R01 AG027388
6 · The paper itself

Abstract

AP-2alpha and c-MYC are important transcription factors involved in multiple cellular processes. They each display the paradoxical capacities to stimulate both cell proliferation and apoptosis under different conditions. In the present study we found that over expression of c-MYC was associated with accumulation of reactive oxygen species (ROS) and apoptosis in human keratinocytes, both of which were significantly inhibited by co-expression of AP-2. The effects of AP-2 on c-MYC were active at several levels. First, AP-2 and c-MYC were confirmed to interact at the protein level as previously described. In addition, forced expression of AP-2 significantly decreased steady state levels of c-MYC mRNA and protein. These findings suggested that AP-2 may have a direct effect on the c-myc gene. Chromatin immunoprecipitation assays demonstrated that AP-2 proteins bound to a cluster of AP-2 binding sites located within a 2 kb upstream regulatory region of c-myc These results suggest that the negative regulation of AP-2 on c-MYC activity was achieved through binding of AP-2 protein to the c-myc gene. The effects of AP-2 on c-MYC induced ROS accumulation and apoptosis in epidermal keratinocytes are likely to play an important role in cell growth, differentiation and carcinogenesis of the skin.

Identifiers

PMID20066163
PMCPMC2801504
OpenAlexW2133131723

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.