Evidence map›Paper›PMID 20980435›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2010

Mechanisms of progesterone receptor inhibition of inflammatory responses in cellular models of breast cancer.

Sakiko Kobayashi, James P Stice, Dmitri Kazmin, Bryan M Wittmann, Erin A Kimbrel, Dean P Edwards, Ching-Yi Chang, Donald P McDonnell

Open access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

21 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. The Dysregulated Pharmacology of Clinically RelevantMolecular cancer therapeutics · 2020
    Article
  6. Article
  7. Article
  8. Steroid receptor/coactivator binding inhibitors: An update.Molecular and cellular endocrinology · 2019
    Review
  9. Progesterone activation of zebrafish mineralocorticoid receptor may influence growth of some transplanted tumors.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
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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

8 authors at 4 institutions in 1 country.

Sakiko KobayashiDepartment of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710, USA.
James P Stice
Dmitri Kazmin
Bryan M Wittmann
Erin A Kimbrel
Dean P Edwards
Ching-Yi Chang
Donald P McDonnell
Duke Medical Center · USDuke University · USBaylor College of Medicine · USDuke University Hospital · US

Funding

Mechanism of Action of Estrogens and AntiestrogensR37DK048807 · NIDDK · DUKE UNIVERSITY · PI MCDONNELL, DONALD P · 2005 to 2014
$5.0M
MECHANISM OF ESTROGENS AND ANTIESTROGENSR01DK048807 · NIDDK · DUKE UNIVERSITY · PI MCDONNELL, DONALD P · 1995 to 2019
$4.3M
The pharmacological actions of antiprogestins in uterine fibroidsR01HD058640 · NICHD · DUKE UNIVERSITY · PI MCDONNELL, DONALD P · 2009 to 2010
$817k
NICHD NIH HHS HD058640NICHD NIH HHS R01 HD058640NIDDK NIH HHS DK048807NIDDK NIH HHS R01 DK048807NIDDK NIH HHS R37 DK048807
6 · The paper itself

Abstract

Both pro- and antimitogenic activities have been ascribed to progesterone receptor (PR) agonists and antagonists in breast cancer cells; however, the transcriptional responses that underlie these paradoxical functions are not apparent. Using nontransformed, normal human mammary epithelial cells engineered to express PR and standard microarray technology, we defined 2370 genes that were significantly regulated by the PR agonist R5020. Gene ontology (GO) analysis revealed that GO terms involved in inflammation and nuclear factor-κB (NF-κB) signaling were among the most significantly regulated. Interestingly, on those NF-κB responsive genes that were inhibited by agonist-activated PR, antagonists either 1) mimicked the actions of agonists or 2) reversed the inhibitory actions of agonists. This difference in pharmacological response could be attributed to the fact that although agonist- and antagonist-activated PR is recruited to NF-κB-responsive promoters, the physical presence of PR tethered to the promoter of some genes is sufficient for transcriptional inhibition, whereas on others, an agonist-activated PR conformation is required for inhibition of NF-κB signaling. Importantly, the actions of PR on the latter class of genes were reversed by an activation function-2-inhibiting, LXXLL-containing peptide. Consideration of the relative activities of these distinct antiinflammatory pathways in breast cancer may be instructive with respect to the likely therapeutic activity of PR agonists or antagonists in the treatment of breast cancer.

Indexed as

Amino Acid SequenceCell LineCell Line, TumorEnhancer Elements, GeneticEpithelial CellsFemaleGonanesHumansInflammatory Breast NeoplasmsInterleukin-1betaMifepristoneMolecular Sequence DataNF-kappa BProgesteroneProgestinsPromoter Regions, GeneticGonanesInterleukin-1betaMifepristoneNF-kappa BonapristoneProgesteroneProgestinsProtein IsoformsReceptors, ProgesteroneRNA, Messenger

Identifiers

PMID20980435
PMCPMC2999472
OpenAlexW2411761847

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.