Evidence map›Paper›PMID 23821771›Full record

ArticleScience signaling2013

Estrogen alters the splicing of type 1 corticotropin-releasing hormone receptor in breast cancer cells.

Suchita Lal, Anna Allan, Danijela Markovic, Rosemary Walker, James Macartney, Nick Europe-Finner, Alison Tyson-Capper, Dimitris K Grammatopoulos

Abstract read
PubMed Publisher
In one paragraph

Article in Science signaling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.6field-weighted citation impact, top 15% 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

17 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Sex-Related Predisposition to Post-Traumatic Stress Disorder Development-The Role of Neuropeptides.International journal of environmental research and public health · 2021
    Review
  5. Targeting Splicing Factor SRSF6 for Cancer Therapy.Frontiers in cell and developmental biology · 2021
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. The clock protein period 2 synchronizes mitotic expansion and decidual transformation of human endometrial stromal cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015
    Article
  16. CRH-R splicing in estrogen-sensitive breast cancer.Cell cycle (Georgetown, Tex.) · 2014
    Article
  17. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Suchita LalDivision of Metabolic and Vascular Health, Warwick Medical School, University of Warwick, Gibbet Hill Road, Coventry CV4 7AL, UK.
Anna Allan
Danijela Markovic
Rosemary Walker
James Macartney
Nick Europe-Finner
Alison Tyson-Capper
Dimitris K Grammatopoulos
California Institute of Technology · US

Funding

Wellcome Trust
6 · The paper itself

Abstract

Hormonal stress response is associated with the pathogenesis of disease, including cancer. The role of the stress hormone CRH (corticotropin-releasing hormone) in breast cancer is complex, and its abundance and biological activity may be modulated by estrogen. In the estrogen receptor-positive (ER+) malignant mammary epithelial cell line MCF7, CRH activated numerous kinases and downstream effectors, at least some of which were mediated by the CRH receptor type 1 (CRH-R1). CRH also increased the transcription of many genes that encode effectors, transcriptional targets, or regulators associated with estrogen signaling. Estrogen increased the abundance of the mRNA encoding CRH-R2 and an alternative splice variant encoding CRH-R1 in which exon 12 was deleted [CRH-R1(Δ12)]. Estrogen inhibited the expression SRSF6, which encodes serine/arginine-rich splicing factor 55 (SRp55). An increase in CRH-R1(Δ12), in response to either estrogen or SRp55 knockdown, dampened the cellular response to CRH and prevented its inhibitory effects on cell invasion. SRp55 knockdown also induced additional splicing events within exons 9 to 12 of CRH-R1, whereas overexpression of SRp55 prevented estrogen-induced generation of CRH-R1(Δ12). ER+ breast tumors had increased CRH-R2 and CRH-R1(Δ12) mRNA abundance, which was associated with decreased abundance of the mRNA encoding SRp55, compared with the amounts in ER- tumors, suggesting that estrogen contributes to the pathophysiology of ER+ breast cancer by altering CRH receptor diversity and disrupting CRH-mediated signaling.

Indexed as

Alternative SplicingBlotting, WesternBreast NeoplasmsCell MovementCorticotropin-Releasing HormoneCRF Receptor, Type 1EstrogensGene Expression Regulation, NeoplasticGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansMCF-7 CellsMicroscopy, ConfocalMitogen-Activated Protein KinasesNuclear ProteinsPhosphoproteinsCorticotropin-Releasing HormoneCRF Receptor, Type 1CRF receptor type 2EstrogensGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaMitogen-Activated Protein KinasesNuclear ProteinsPhosphoproteinsReceptors, Corticotropin-Releasing HormoneReceptors, EstrogenRNA-Binding ProteinsSerine-Arginine Splicing FactorsSRSF6 protein, human

Identifiers

PMID23821771
OpenAlexW2161570432

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.