Evidence map›Paper›PMID 30375476›Full record

ArticleScientific reports2018

Metabotropic glutamate receptor-1 regulates inflammation in triple negative breast cancer.

Rachel E Sexton, Ali H Hachem, Ali A Assi, Miriam A Bukhsh, David H Gorski, Cecilia L Speyer

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.8field-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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. G protein-coupled receptors: a gateway to targeting oncogenic EVs?Extracellular vesicles and circulating nucleic acids · 2024
    Review
  5. The tumor-nerve circuit in breast cancer.Cancer metastasis reviews · 2023
    Review
  6. Review
  7. Review
  8. Review
  9. Cell Trafficking at the Intersection of the Tumor-Immune Compartments.Annual review of biomedical engineering · 2022
    Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
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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

6 authors at 4 institutions in 1 country.

Rachel E SextonCancer Biology Graduate Program, Wayne State University, Barbara Ann Karmanos Cancer Institute, 4100 John R St., Detroit, MI, 48201, USA.
Ali H HachemCentral Michigan University College of Medicine, 1000 Houghton Ave., Saginaw, MI, 48602, USA.
Ali A AssiUniversity of Michigan School of Medicine, M4101 Medical Science Building I - C Wing, 1301 Catherine St., Ann Arbor, MI, 48109-5624, USA.
Miriam A BukhshOakland University William Beaumont School of Medicine, 2200 N. Squirrel Road, Rochester, MI, 48309, USA.
David H GorskiMichael and Marian Ilitch Department of Surgery, Wayne State University School of Medicine, Barbara Ann Karmanos Cancer Institute, 4100 John R St., Detroit, MI, 48201, USA.ORCID http://orcid.org/0000-0002-9805-6699
Cecilia L SpeyerMichael and Marian Ilitch Department of Surgery, Wayne State University School of Medicine, Barbara Ann Karmanos Cancer Institute, 4100 John R St., Detroit, MI, 48201, USA. clspeyer@wayne.edu.
Wayne State University · USCentral Michigan University · USOakland University · USUniversity of Michigan · US

Funding

Tumor Biology and Microenvironment (Program 1)P30CA022453 · NCI · WAYNE STATE UNIVERSITY · PI PAUL M STEMMER · 1985 to 2026
$68.4M
NCI NIH HHS P30 CA02245NCI NIH HHS P30 CA022453
6 · The paper itself

Abstract

Breast cancer remains a major cause of death among women. 15% of these cancers are triple negative breast cancer (TNBC), an aggressive subtype of breast cancer for which no current effective targeted therapy exists. We have previously demonstrated a role for mGluR1 in mediating tumor cell growth, endothelial cell proliferation, and tumor-induced angiogenesis in TNBC. In this study, we explore a role for mGluR1 in regulating inflammation in TNBC. GRM1 expression was silenced in MDA-MB-231 cells to study changes in expression of inflammatory genes regulated by mGluR1. Results were confirmed by ELISA using GRM1-silenced and overexpressed cells and mGluR1 inhibitors. A functional role for these differentially expressed genes was determined in vitro and in vivo. 131 genes were differentially expressed in GRM1-silenced MDA-MB-231 cells, with some of these falling into four major canonical pathways associated with acute inflammation, specifically leukocyte migration/chemotaxis. Upregulation of three of these genes (CXCL1, IL6, IL8) and their corresponding protein was confirmed by qPCR analysis and ELISA in GRM1-manipulated TNBC cells. Upregulation of these cytokines enhanced endothelial adhesion and transmigration of neutrophils in co-culture assays and in 4T1 mouse tumors. Our results suggest mGluR1 may serve as a novel endogenous regulator of inflammation in TNBC.

Indexed as

AnimalsCell CycleCell Line, TumorCell MovementCell ProliferationEnzyme-Linked Immunosorbent AssayGene Expression Regulation, NeoplasticHumansInflammationMiceReceptors, Metabotropic GlutamateSignal TransductionTriple Negative Breast NeoplasmsXenograft Model Antitumor Assaysmetabotropic glutamate receptor type 1Receptors, Metabotropic Glutamate

Identifiers

PMID30375476
PMCPMC6207734
OpenAlexW2898122647

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.