Evidence map›Paper›PMID 34299224›Full record

ArticleInternational journal of molecular sciences2021

ERα36-GPER1 Collaboration Inhibits TLR4/NFκB-Induced Pro-Inflammatory Activity in Breast Cancer Cells.

George Notas, Athanasios Panagiotopoulos, Rodanthi Vamvoukaki, Konstantina Kalyvianaki, Foteini Kiagiadaki, Alexandra Deli, Marilena Kampa, Elias Castanas

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

14 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2025
    Article
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  8. Pig-Derived ProbioticAnimals : an open access journal from MDPI · 2024
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
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 1 institution in 1 country.

George NotasLaboratory of Experimental Endocrinology, School of Medicine, University of Crete, 71500 Heraklion, Greece.ORCID 0000-0002-2506-5252
Athanasios PanagiotopoulosLaboratory of Experimental Endocrinology, School of Medicine, University of Crete, 71500 Heraklion, Greece.
Rodanthi VamvoukakiLaboratory of Experimental Endocrinology, School of Medicine, University of Crete, 71500 Heraklion, Greece.ORCID 0000-0002-7798-6264
Konstantina KalyvianakiLaboratory of Experimental Endocrinology, School of Medicine, University of Crete, 71500 Heraklion, Greece.ORCID 0000-0002-2145-9430
Foteini KiagiadakiLaboratory of Experimental Endocrinology, School of Medicine, University of Crete, 71500 Heraklion, Greece.
Alexandra DeliLaboratory of Experimental Endocrinology, School of Medicine, University of Crete, 71500 Heraklion, Greece.
Marilena KampaLaboratory of Experimental Endocrinology, School of Medicine, University of Crete, 71500 Heraklion, Greece.
Elias CastanasLaboratory of Experimental Endocrinology, School of Medicine, University of Crete, 71500 Heraklion, Greece.ORCID 0000-0002-8370-1835
University of Crete · GR

Funding

Deutscher Akademischer Austauschdienst 57515112Foundation for Education and European Culture research fund n/aUniversity of Crete 3442
6 · The paper itself

Abstract

Inflammation is important for the initiation and progression of breast cancer. We have previously reported that in monocytes, estrogen regulates TLR4/NFκB-mediated inflammation via the interaction of the Erα isoform ERα36 with GPER1. We therefore investigated whether a similar mechanism is present in breast cancer epithelial cells, and the effect of ERα36 expression on the classic 66 kD ERα isoform (ERα66) functions. We report that estrogen inhibits LPS-induced NFκB activity and the expression of downstream molecules TNFα and IL-6. In the absence of ERα66, ERα36 and GPER1 are both indispensable for this effect. In the presence of ERα66, ERα36 or GPER1 knock-down partially inhibits NFκB-mediated inflammation. In both cases, ERα36 overexpression enhances the inhibitory effect of estrogen on inflammation. We also verify that ERα36 and GPER1 physically interact, especially after LPS treatment, and that GPER1 interacts directly with NFκB. When both ERα66 and ERα36 are expressed, the latter acts as an inhibitor of ERα66 via its binding to estrogen response elements. We also report that the activation of ERα36 leads to the inhibition of breast cancer cell proliferation. Our data support that ERα36 is an inhibitory estrogen receptor that, in collaboration with GPER1, inhibits NFκB-mediated inflammation and ERα66 actions in breast cancer cells.

Indexed as

Breast NeoplasmsCell Line, TumorEpithelial CellsEstradiolEstrogen Receptor alphaEstrogensFemaleGene Expression Regulation, NeoplasticHumansInflammationInterleukin-6MCF-7 CellsMonocytesNF-kappa BReceptors, EstrogenReceptors, G-Protein-CoupledESR1 protein, humanEstradiolEstrogen Receptor alphaestrogen receptor alpha 36, humanEstrogensGPER1 protein, humanInterleukin-6NF-kappa BReceptors, EstrogenReceptors, G-Protein-CoupledToll-Like Receptor 4Tumor Necrosis Factor-alphabreast cancerestrogen receptor alpha 36GPER1IL-6NF-κBTLR4TNFα

Identifiers

PMID34299224
PMCPMC8303269
OpenAlexW3179419163

What OpenQuestion holds

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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.