Evidence map›Paper›PMID 20705611›Full record

ArticleThe Journal of biological chemistry2010

Proinflammatory cytokines enhance estrogen-dependent expression of the multidrug transporter gene ABCG2 through estrogen receptor and NF{kappa}B cooperativity at adjacent response elements.

Madhumita Pradhan, Leslie A Bembinster, Sarah C Baumgarten, Jonna Frasor

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 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
4.1field-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

51 citing papers in PubMed, 90 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Multidrug efflux transporter ABCG2: expression and regulation.Cellular and molecular life sciences : CMLS · 2021
    Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Interaction of the p.Q141K Variant of theJournal of clinical medicine · 2019
    Article
  17. Article
  18. Article
  19. Rare Variants in theDrug metabolism and disposition: the biological fate of chemicals · 2018
    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

4 authors at 1 institution in 1 country.

Madhumita PradhanDepartment of Physiology and Biophysics, University of Illinois at Chicago, Chicago, Illinois 60612, USA.
Leslie A Bembinster
Sarah C Baumgarten
Jonna Frasor
University of Illinois Chicago · US

Funding

TRAINING IN CELLULAR SIGNALLING IN THE CARDIOVASCULAR SYT32HL007692 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI SOLARO, R JOHN · 1990 to 2014
$8.5M
Crosstalk between estrogen receptor and NFkB in target gene regulationR01CA130932 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI FRASOR, JONNA · 2009 to 2013
$1.5M
NCI NIH HHS CA130932-2NCI NIH HHS R01 CA130932NHLBI NIH HHS T32 HL007692
6 · The paper itself

Abstract

Constitutive activation of NFκB in estrogen receptor (ER)-positive breast cancer is associated with tumor recurrence and development of anti-estrogen resistance. Furthermore, a gene expression signature containing common targets for ER and NFκB has been identified and found to be associated with the more aggressive luminal B intrinsic subtype of ER-positive breast tumors. Here, we describe a novel mechanism by which ER and NFκB cooperate to up-regulate expression of one important gene from this signature, ABCG2, which encodes a transporter protein associated with the development of drug-resistant breast cancer. We and others have confirmed that this gene is regulated primarily by estrogen in an ER- and estrogen response element (ERE)-dependent manner. We found that whereas proinflammatory cytokines have little effect on this gene in the absence of 17β-estradiol, they can potentiate ER activity in an NFκB-dependent manner. ER allows the NFκB family member p65 to access a latent NFκB response element located near the ERE in the gene promoter. NFκB recruitment to the gene is, in turn, required to stabilize ER occupancy at the functional ERE. The result of this cooperative binding of ER and p65 at adjacent response elements leads to a major increase in both ABCG2 mRNA and protein expression. These findings indicate that estrogen and inflammatory factors can modify each other's activity through modulation of transcription factor accessibility and/or occupancy at adjacent response elements. This novel transcriptional mechanism could have important implications in breast cancer, where both inflammation and estrogen can promote cancer progression.

Indexed as

Drug Resistance, NeoplasmGene Expression Regulation, NeoplasticResponse ElementsATP-Binding Cassette TransportersATP Binding Cassette Transporter, Subfamily G, Member 2Breast NeoplasmsCell Line, TumorCytokinesEstradiolEstrogensFemaleHumansNeoplasm ProteinsReceptors, EstrogenRNA, MessengerTranscription Factor RelAABCG2 protein, humanATP-Binding Cassette TransportersATP Binding Cassette Transporter, Subfamily G, Member 2CytokinesEstradiolEstrogensNeoplasm ProteinsReceptors, EstrogenRELA protein, humanRNA, MessengerTranscription Factor RelA

Identifiers

PMID20705611
PMCPMC2951183
OpenAlexW1967759358

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.