Evidence map›Paper›PMID 17910036›Full record

ArticleJournal of cellular biochemistry2008

Deregulation of cofactor of BRCA1 expression in breast cancer cells.

Jianlong Sun, Gareth Watkins, Ashley L Blair, Christopher Moskaluk, Sagar Ghosh, Wen G Jiang, Rong Li

Open access · greenAbstract read
In one paragraph

Article in Journal of cellular biochemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

27 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
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  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Negative elongation factor is essential for endometrial function.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  11. Article
  12. Article
  13. RNA polymerase II pausing as a context-dependent reader of the genome.Biochemistry and cell biology = Biochimie et biologie cellulaire · 2016
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Glucocorticoid receptor represses proinflammatory genes at distinct steps of the transcription cycle.Proceedings of the National Academy of Sciences of the United States of America · 2013
    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 3 institutions in 2 countries.

Jianlong SunDepartment of Molecular Medicine, Institute of Biotechnology, 15355 Lambda Drive, University of Texas Health Science Center at San Antonio, San Antonio, Texas 78245, USA.
Gareth Watkins
Ashley L Blair
Christopher Moskaluk
Sagar Ghosh
Wen G Jiang
Rong Li
Cardiff University · GBUniversity of Virginia · USThe University of Texas Health Science Center at San Antonio · US

Funding

A Novel Corepressor of Estrogen ReceptorR01DK064604 · NIDDK · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI LI, RONG · 2004 to 2007
$1.0M
NIDDK NIH HHS DK064604NIDDK NIH HHS R01 DK064604
6 · The paper itself

Abstract

Cofactor of BRCA1 (COBRA1) is an integral component of the human negative elongation factor (NELF), a four-subunit protein complex that inhibits transcription elongation. Previous in vivo work indicates that COBRA1 and the rest of the NELF complex repress estrogen-dependent transcription and the growth of breast cancer cells. In light of the COBRA1 function in breast cancer-related gene expression, we sought to examine regulation of COBRA1 expression in both established breast cancer cell lines and breast carcinoma tissues. We found that COBRA1 expression was inversely correlated with breast cancer progression, as tumor samples of patients who had distant metastasis and local recurrence expressed very low levels of COBRA1 mRNA when compared to those who were disease free for over 10 years (P = 0.0065 and 0.0081, respectively). Using both breast and prostate cancer cell lines, we also explored the possible mechanisms by which COBRA1 expression is regulated. Our results indicate that the protein abundance of COBRA1 and the other NELF subunits are mutually influenced in a tightly coordinated fashion. Small interfering RNA (siRNA) that targeted at one NELF subunit dampened the protein levels of all four subunits. Conversely, ectopic expression of COBRA1 in the knockdown cells partially rescues the co-depletion of the NELF subunits. In addition, our study suggests that a post-transcriptional, proteasome-independent mechanism is involved in the interdependent regulation of the NELF abundance. Furthermore, a lack of COBRA1 expression in breast carcinoma may serve as a useful indicator for poor prognosis.

Indexed as

Biomarkers, TumorBreast NeoplasmsCell Line, TumorFemaleHumansMaleNeoplasm MetastasisNuclear ProteinsProstatic NeoplasmsRNA, MessengerTranscription FactorsBiomarkers, Tumornegative elongation factorNSMF protein, humanNuclear ProteinsRNA, MessengerTranscription Factors

Identifiers

PMID17910036
PMCPMC8822876
OpenAlexW2039050926

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.