Evidence map›Paper›PMID 30051594›Full record

ArticleMolecular oncology2018

Feedback control of the CXCR7/CXCL11 chemokine axis by estrogen receptor α in ovarian cancer.

Samira Benhadjeba, Lydia Edjekouane, Karine Sauvé, Euridice Carmona, André Tremblay

Open access · goldAbstract read
In one paragraph

Article in Molecular oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 5% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

  1. Pooled it
  2. Review
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  5. Article
  6. Article
  7. Review
  8. Review
  9. Sex Bias in Differentiated Thyroid Cancer.International journal of molecular sciences · 2021
    Review
  10. Article
  11. Review
  12. Article
  13. CXCL12 Signaling in the Tumor Microenvironment.Advances in experimental medicine and biology · 2021
    Review
  14. Article
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  16. 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

5 authors at 1 institution in 1 country.

Samira BenhadjebaResearch Center, CHU Sainte-Justine, Montréal, Canada.
Lydia EdjekouaneResearch Center, CHU Sainte-Justine, Montréal, Canada.
Karine SauvéResearch Center, CHU Sainte-Justine, Montréal, Canada.
Euridice CarmonaCHUM Research Center, Institut du Cancer de Montréal, Canada.
André TremblayResearch Center, CHU Sainte-Justine, Montréal, Canada.ORCID 0000-0003-1547-9846
Centre Hospitalier Universitaire Sainte-Justine · CA

Funding

CIHR
6 · The paper itself

Abstract

Ovarian cancer (OC) is one of the most intractable diseases, exhibiting tremendous molecular heterogeneity and lacking reliable methods for screening, resulting in late diagnosis and widespread peritoneal dissemination. Menopausal estrogen replacement therapy is a well-recognized risk factor for OC, but little is known about how estrogen might contribute to this disease at the cellular level. This study identifies chemokine receptor CXCR7/ACKR3 as an estrogen-responsive gene, whose expression is markedly enhanced by estrogen through direct recruitment of ERα and transcriptional active histone modifications in OC cells. The gene encoding CXCR7 chemokine ligand I-TAC/CXCL11 was also upregulated by estrogen, resulting in Ser-118 phosphorylation, activation, and recruitment of estrogen receptor ERα at the CXCR7 promoter locus for positive feedback regulation. Both CXCR7 and CXCL11, but not CXCR3 (also recognized to interact with CXCL11), were found to be significantly increased in stromal sections of microdissected tumors and positively correlated in mesenchymal subtype of OC. Estrogenic induction of mesenchymal markers SNAI1, SNAI2, and CDH2 expression, with a consequent increase in cancer cell migration, was shown to depend on CXCR7, indicating a key role for CXCR7 in mediating estrogen upregulation of mesenchymal markers to induce invasion of OC cells. These findings identify a feed-forward mechanism that sustains activation of the CXCR7/CXCL11 axis under ERα control to induce the epithelial-mesenchymal transition pathway and metastatic behavior of OC cells. Such interplay underlies the complex gene profile heterogeneity of OC that promotes changes in tumor microenvironment and metastatic acquisition.

Indexed as

Feedback, PhysiologicalBinding SitesCell Line, TumorCell MovementChemokine CXCL11ChromatinEpithelial-Mesenchymal TransitionEstrogen Receptor alphaEstrogensFemaleGene Expression Regulation, NeoplasticGenetic LociHumansMesodermOvarian NeoplasmsPhosphorylationACKR3 protein, humanChemokine CXCL11ChromatinEstrogen Receptor alphaEstrogensPhosphoserineReceptors, CXCRACKR3chemokine receptorsESR1estrogen receptorsovarian cancer mesenchymal subtypestromal compartment

Identifiers

PMID30051594
PMCPMC6165996
OpenAlexW2884084635

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.