Evidence map›Paper›PMID 20075077›Full record

ArticleThe Journal of biological chemistry2010

Foxp3 expression in p53-dependent DNA damage responses.

Da-Jung Jung, Dong-Hoon Jin, Seung-Woo Hong, Jee-Eun Kim, Jae-Sik Shin, Daejin Kim, Byung-Joo Cho, Young-Il Hwang, Jae-Seung Kang, Wang-Jae Lee

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

29 citing papers in PubMed, 62 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Postepy dermatologii i alergologii · 2021
    Article
  6. Article
  7. Review
  8. P53: A Guardian of Immunity Becomes Its Saboteur through Mutation.International journal of molecular sciences · 2020
    Review
  9. Review
  10. Article
  11. Article
  12. Long noncoding RNAs in the p53 network.Wiley interdisciplinary reviews. RNA · 2017
    Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Clinical significance of FOXP3 expression in human gliomas.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2014
    Article
  20. Review
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

10 authors at 4 institutions in 1 country.

Da-Jung JungDepartment of Anatomy and Tumor Immunity Medical Research Center, Seoul National University College of Medicine, Seoul 110-744, USA.
Dong-Hoon Jin
Seung-Woo Hong
Jee-Eun Kim
Jae-Sik Shin
Daejin Kim
Byung-Joo Cho
Young-Il Hwang
Jae-Seung Kang
Wang-Jae Lee
Seoul National University · KRSeoul National University Hospital · KRChung-Ang University · KRKonkuk University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The forkhead transcription factor, Foxp3, is thought to act as a master regulator that controls (suppresses) expression of the breast cancer oncogenes, SKP2 and HER-2/ErbB2. However, the mechanisms that regulate Foxp3 expression and thereby modulate tumor development remain largely unexplored. Here, we demonstrate that Foxp3 up-regulation requires p53 function, showing that Foxp3 expression is directly regulated by p53 upon DNA damage responses in human breast and colon carcinoma cells. Treatment with the genotoxic agents, doxorubicin or etoposide, induced Foxp3 expression in p53-positive carcinoma cells, but not in cells lacking p53 function. Furthermore, knock down of endogenous wild-type p53 using RNA interference abrogated Foxp3 induction by genotoxic agents, and exogenous expression of p53 in cells lacking p53 restored the responsiveness of Foxp3 to DNA-damaging stresses. In addition, Foxp3 knock down blunted the p53-mediated growth inhibitory response to DNA-damaging agents. These results suggest that induction of Foxp3 in the context of tumor suppression is regulated in a p53-dependent manner and implicate Foxp3 as a key determinant of cell fate in p53-dependent DNA damage responses.

Indexed as

Antibiotics, AntineoplasticAntineoplastic Agents, PhytogenicBreast NeoplasmsCell DeathCell DivisionColonic NeoplasmsDNA DamageDoxorubicinEtoposideFemaleForkhead Transcription FactorsGene Expression Regulation, NeoplasticHCT116 CellsHumansImidazolesPhosphorylationAntibiotics, AntineoplasticAntineoplastic Agents, PhytogenicDoxorubicinEtoposideForkhead Transcription FactorsFOXP3 protein, humanImidazolesMDM2 protein, humannutlin 3PiperazinesProto-Oncogene Proteins c-mdm2Tumor Suppressor Protein p53

Identifiers

PMID20075077
PMCPMC2832950
OpenAlexW2120313198

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.