Evidence map›Paper›PMID 29996493›Full record

ReviewInternational journal of molecular sciences2018

Crosstalk between Notch, HIF-1α and GPER in Breast Cancer EMT.

Ernestina M De Francesco, Marcello Maggiolini, Anna Maria Musti

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed, 1 pooled it
6.3field-weighted citation impact, top 2% 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

84 citing papers in PubMed, 1 synthesis or guideline pooled it, 146 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Effects of NaCell biochemistry and biophysics · 2025
    Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review

24 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 2 countries.

Ernestina M De FrancescoDepartment of Pharmacy, Health and Nutritional Sciences, University of Calabria, 87036 Rende, Italy. ernestina.defrancesco@manchester.ac.uk.
Marcello MaggioliniDepartment of Pharmacy, Health and Nutritional Sciences, University of Calabria, 87036 Rende, Italy. marcellomaggiolini@yahoo.it.ORCID 0000-0002-7485-854X
Anna Maria MustiDepartment of Pharmacy, Health and Nutritional Sciences, University of Calabria, 87036 Rende, Italy. annamaria.musti@unical.it.ORCID 0000-0003-1443-2739
University of Calabria · ITBreast Cancer Now · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Notch signaling pathway acts in both physiological and pathological conditions, including embryonic development and tumorigenesis. In cancer progression, diverse mechanisms are involved in Notch-mediated biological responses, including angiogenesis and epithelial-mesenchymal-transition (EMT). During EMT, the activation of cellular programs facilitated by transcriptional repressors results in epithelial cells losing their differentiated features, like cell–cell adhesion and apical–basal polarity, whereas they gain motility. As it concerns cancer epithelial cells, EMT may be consequent to the evolution of genetic/epigenetic instability, or triggered by factors that can act within the tumor microenvironment. Following a description of the Notch signaling pathway and its major regulatory nodes, we focus on studies that have given insights into the functional interaction between Notch signaling and either hypoxia or estrogen in breast cancer cells, with a particular focus on EMT. Furthermore, we describe the role of hypoxia signaling in breast cancer cells and discuss recent evidence regarding a functional interaction between HIF-1α and GPER in both breast cancer cells and cancer-associated fibroblasts (CAFs). On the basis of these studies, we propose that a functional network between HIF-1α, GPER and Notch may integrate tumor microenvironmental cues to induce robust EMT in cancer cells. Further investigations are required in order to better understand how hypoxia and estrogen signaling may converge on Notch-mediated EMT within the context of the stroma and tumor cells interaction. However, the data discussed here may anticipate the potential benefits of further pharmacological strategies targeting breast cancer progression.

Indexed as

Breast NeoplasmsCell Line, TumorDisease ProgressionEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansHypoxia-Inducible Factor 1, alpha SubunitReceptor Cross-TalkReceptors, EstrogenReceptors, G-Protein-CoupledReceptors, NotchSignal TransductionGPER1 protein, humanHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitReceptors, EstrogenReceptors, G-Protein-CoupledReceptors, Notchbreast cancercancer associated fibroblastEMTestrogenGPERhypoxianotch signaling

Identifiers

PMID29996493
PMCPMC6073901
OpenAlexW2826708737

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.