Evidence map›Paper›PMID 33212987›Full record

ArticleInternational journal of molecular sciences2020

Glucose Concentration in Cell Culture Medium Influences the BRCA1-Mediated Regulation of the Lipogenic Action of IGF-I in Breast Cancer Cells.

Moses O Koobotse, Dayane Schmidt, Jeff M P Holly, Claire M Perks

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 17% 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, 25 citations in OpenAlex.

  1. Article
  2. Review
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  9. Cellular Pre-Adaptation to the High OAntioxidants (Basel, Switzerland) · 2024
    Article
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  15. Article
  16. BRCA1: An Endocrine and Metabolic Regulator.Frontiers in endocrinology · 2022
    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

4 authors at 2 institutions in 2 countries.

Moses O KoobotseIGFs & Metabolic Endocrinology Group, Bristol Medical School, Translational Health Sciences, University of Bristol, Bristol BS10 5NB, UK.ORCID 0000-0001-6065-0986
Dayane SchmidtIGFs & Metabolic Endocrinology Group, Bristol Medical School, Translational Health Sciences, University of Bristol, Bristol BS10 5NB, UK.
Jeff M P HollyIGFs & Metabolic Endocrinology Group, Bristol Medical School, Translational Health Sciences, University of Bristol, Bristol BS10 5NB, UK.
Claire M PerksIGFs & Metabolic Endocrinology Group, Bristol Medical School, Translational Health Sciences, University of Bristol, Bristol BS10 5NB, UK.
University of Bristol · GBUniversity of Botswana · BW

Funding

Cancer Research UK 19169Cancer Research UK C18281/A19169
6 · The paper itself

Abstract

Hyperglycaemia is a common metabolic alteration associated with breast cancer risk and progression. We have previously reported that BRCA1 restrains metabolic activity and proliferative response to IGF-I anabolic actions in breast cancer cells cultured in high glucose. Here, we evaluated the impact of normal physiological glucose on these tumour suppressive roles of BRCA1. Human breast cancer cells cultured in normal physiological and high glucose were treated with IGF-I (0-500 ng/mL). Cellular responses were evaluated using immunoblotting, co-immunoprecipitation, and cell viability assay. As we previously reported, IGF-I induced ACCA dephosphorylation by reducing the association between BRCA1 and phosphorylated ACCA in high glucose, and upregulated FASN abundance downstream of ACCA. However, these effects were not observed in normal glucose. Normal physiological glucose conditions completely blocked IGF-I-induced ACCA dephosphorylation and FASN upregulation. Co-immunoprecipitation studies showed that normal physiological glucose blocked ACCA dephosphorylation by increasing the association between BRCA1 and phosphorylated ACCA. Compared to high glucose, the proliferative response of breast cancer cells to IGF-I was reduced in normal glucose, whereas no difference was observed in normal mammary epithelial cells. Considering these results collectively, we conclude that normal physiological glucose promotes the novel function of BRCA1 as a metabolic restraint of IGF-I actions. These data suggest that maintaining normal glucose levels may improve BRCA1 function in breast cancer and slow down cancer progression.

Indexed as

BRCA1 ProteinBreast NeoplasmsCell ProliferationCulture MediaFatty Acid Synthase, Type IFemaleGlucoseHumansInsulin-Like Growth Factor ILipogenesisMCF-7 CellsPhosphorylationReceptors, G-Protein-CoupledBRCA1 ProteinBRCA1 protein, humanCulture MediaFASN protein, humanFatty Acid Synthase, Type IGlucoseGPR3 protein, humanIGF1 protein, humanInsulin-Like Growth Factor IReceptors, G-Protein-CoupledBRCA1breast cancerfatty acid synthesishyperglycaemiaIGF-I

Identifiers

PMID33212987
PMCPMC7698585
OpenAlexW3102082137

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.