Evidence map›Paper›PMID 22167187›Full record

ArticleThe Journal of biological chemistry2012

p21 cooperates with DDB2 protein in suppression of ultraviolet ray-induced skin malignancies.

Tanya Stoyanova, Nilotpal Roy, Shaumick Bhattacharjee, Dragana Kopanja, Ted Valli, Srilata Bagchi, Pradip Raychaudhuri

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

24 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Expression of CD44Gynecologic oncology reports · 2022
    Article
  6. Revisiting the Function of p21International journal of molecular sciences · 2022
    Review
  7. Article
  8. Article
  9. Article
  10. Emerging Roles of DDB2 in Cancer.International journal of molecular sciences · 2019
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  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 2 institutions in 1 country.

Tanya StoyanovaDepartment of Biochemistry and Molecular Genetics, Cancer Center, University of Illinois at Chicago, Chicago, Illinois 60607, USA.
Nilotpal Roy
Shaumick Bhattacharjee
Dragana Kopanja
Ted Valli
Srilata Bagchi
Pradip Raychaudhuri
University of Illinois Chicago · USIVDiagnostics (United States) · US

Funding

Role of DDB in Checkpoint Control and CarcinogenesisR01CA077637 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI RAYCHAUDHURI, PRADIP · 1999 to 2014
$3.6M
DNA Damage Response and DDBR01CA156164 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI BAGCHI, SRILATA, RAYCHAUDHURI, PRADIP · 2010 to 2014
$1.6M
NCI NIH HHS CA 156164NCI NIH HHS CA77637NCI NIH HHS R01 CA077637NCI NIH HHS R01 CA156164
6 · The paper itself

Abstract

Exposure to ultraviolet rays (UV) in sunlight is the main cause of skin cancer. Here, we show that the p53-induced genes DDB2 and p21 are down-regulated in skin cancer, and in the mouse model they functionally cooperate to prevent UV-induced skin cancer. Our previous studies demonstrated an antagonistic role of DDB2 and p21 in nucleotide excision repair and apoptosis. Surprisingly, we find that the loss of p21 restores nucleotide excision repair and apoptosis in Ddb2(-/-) mice, but it does not protect from UV-mediated skin carcinogenesis. In contrast, Ddb2(-/-)p21(-/-) mice are significantly more susceptible to UV-induced skin cancer than the Ddb2(-/-) or the p21(-/-) mice. We provide evidence that p21 deletion in the Ddb2(-/-) background causes a strong increase in cell proliferation. The increased proliferation in the Ddb2(-/-)p21(-/-) background is related to a severe deficiency in UV-induced premature senescence. Also, the oncogenic pro-proliferation transcription factor FOXM1 is overexpressed in the p21(-/-) background. Our results show that the anti-proliferative and the pro-senescence pathways of DDB2 and p21 are critical protection mechanisms against skin malignancies.

Indexed as

AnimalsCell ProliferationCellular SenescenceCyclin-Dependent Kinase Inhibitor p21DNA-Binding ProteinsDNA RepairForkhead Box Protein M1Forkhead Transcription FactorsGene DeletionMiceMice, KnockoutNeoplasms, Radiation-InducedSkin NeoplasmsTumor Suppressor Protein p53Ultraviolet RaysCdkn1a protein, mouseCyclin-Dependent Kinase Inhibitor p21Ddb2 protein, mouseDNA-Binding ProteinsForkhead Box Protein M1Forkhead Transcription FactorsFoxm1 protein, mouseTumor Suppressor Protein p53

Identifiers

PMID22167187
PMCPMC3270959
OpenAlexW2018117880

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.