Evidence map›Paper›PMID 12700667›Full record

ArticleOncogene2003

p62 overexpression in breast tumors and regulation by prostate-derived Ets factor in breast cancer cells.

H Garrett R Thompson, Joseph W Harris, Barbara J Wold, Fritz Lin, James P Brody

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers.

0numbers the graph read from it
0cells of the map it votes in
105citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

105 citing papers in PubMed, 183 citations in OpenAlex.

  1. Regulation of cell proliferation and migration by p62 through stabilization of Twist1.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Trial
  2. The Roles of SQSTM1/p62 in Selective Autophagy and Oncogenic Signaling.International journal of molecular sciences · 2026
    Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Autophagy and cancer therapy.Cancer letters · 2024
    Review
  8. Review
  9. The sequestosome 1 protein: therapeutic vulnerabilities in ovarian cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Frontiers in nuclear medicine · 2023
    Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

45 more citing papers are in PubMed but not listed here.

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

5 authors at 3 institutions in 1 country.

H Garrett R ThompsonDepartment of Biomedical Engineering, University of California, CA 92697-2715, USA.
Joseph W Harris
Barbara J Wold
Fritz Lin
James P Brody
University of California, Irvine · USCalifornia Institute of Technology · USUniversity of California, Irvine Medical Center · US

Funding

DEVELOPMENT OF GENOMIC INSTRUMENTATIONK22HG000047 · NHGRI · UNIVERSITY OF CALIFORNIA IRVINE · PI BRODY, JAMES P · 2000 to 2004
$964k
NHGRI NIH HHS 1K22HG00047-01NHGRI NIH HHS K22 HG000047
6 · The paper itself

Abstract

p62 is a multifunctional cytoplasmic protein able to noncovalently bind ubiquitin and several signaling proteins, suggesting a regulatory role connected to the ubiquitin-proteasome pathway. No studies to date have linked p62 protein expression with pathological states. Here we demonstrate the overabundance of p62 protein in malignant breast tissue relative to normal breast tissue. The proteasome inhibitor PSI increased p62 mRNA and protein; however, PSI treatment of breast epithelial cells transfected with the p62 promoter did not affect promoter activity. High levels of prostate-derived Ets factor (PDEF) mRNA have been identified in breast cancer compared to normal breast. Only the PSA and maspin promoters have been identified as targets of this transcription factor. Here we show that PDEF stimulates the p62 promoter through at least two sites, and likely acts as a coactivator. PSI treatment abrogates the PDEF-stimulated increase of p62 promoter activity by 50%. Thus, multiple mechanisms for the induction of p62 exist. We conclude that (1) p62 protein is overexpressed in breast cancer; (2) p62 mRNA and protein increase in response to PSI, with no change of basal promoter activity; (3) PDEF upregulates p62 promoter activity through at least two sites; and (4) PSI downregulates PDEF-induced p62 promoter activation through one of these sites.

Indexed as

ProteinsAcetylcysteineAdaptor Proteins, Signal TransducingBreastBreast NeoplasmsCarrier ProteinsCells, CulturedComputer SystemsCysteine EndopeptidasesCysteine Proteinase InhibitorsEpithelial CellsFemaleGene Expression Regulation, NeoplasticHumansLeupeptinsMultienzyme ComplexesAcetylcysteineAdaptor Proteins, Signal Transducingbenzyloxycarbonyl-isoleucyl-glutamyl(O-tert-butyl)-alanyl-leucinalbenzyloxycarbonylleucyl-leucyl-leucine aldehydeCarrier ProteinsCysteine EndopeptidasesCysteine Proteinase InhibitorslactacystinLeupeptinsMultienzyme ComplexesNeoplasm ProteinsOligopeptidesProteasome Endopeptidase ComplexProteinsProto-Oncogene Proteins c-etsRNA, MessengerRNA, NeoplasmSequestosome-1 ProteinSPDEF protein, humanSQSTM1 protein, humanTranscription FactorsUbiquitin

Identifiers

PMID12700667
OpenAlexW1995771017

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.