Evidence map›Paper›PMID 31581558›Full record

ArticleBiomolecules2019

ACSL1 Regulates TNFα-Induced GM-CSF Production by Breast Cancer MDA-MB-231 Cells.

Reeby Thomas, Fatema Al-Rashed, Nadeem Akhter, Fahd Al-Mulla, Rasheed Ahmad

Open access · goldAbstract read
In one paragraph

Article in Biomolecules, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

29 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
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  14. Stage Analysis of Breast Cancer Metabolomics: A System Biology Approach.Asian Pacific journal of cancer prevention : APJCP · 2023
    Article
  15. Article
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  17. Article
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  19. Article
  20. Biomedicines · 2021
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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.

Reeby ThomasMicrobiology & Immunology Department, Dasman Diabetes Institute, Kuwait City, Kuwait. Reeby.Thomas@dasmaninstitute.org.
Fatema Al-RashedMicrobiology & Immunology Department, Dasman Diabetes Institute, Kuwait City, Kuwait. fatema.alrashed@dasmaninstitute.org.
Nadeem AkhterMicrobiology & Immunology Department, Dasman Diabetes Institute, Kuwait City, Kuwait. nadeem.akhter@dasmaninstitute.org.
Fahd Al-MullaGenetics and Bioinformatics Department, Dasman Diabetes Institute, Kuwait City, Kuwait. fahd.almulla@dasmaninstitute.org.
Rasheed AhmadMicrobiology & Immunology Department, Dasman Diabetes Institute, Kuwait City, Kuwait. rasheed.ahmad@dasmaninstitute.org.ORCID 0000-0001-5746-0743
Dasman Diabetes Institute · KW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Overexpression of granulocyte-macrophage colony-stimulating factor (GM-CSF) in different types of cancer is associated with tumor growth and progression. Tumor necrosis factor-α (TNFα) is involved in the induction of GM-CSF in different cells; however, the underlying molecular mechanism in this production of GM-CSF has not been fully revealed. Recently, it was noted that TNFα mediates inflammatory responses through long-chain acyl-CoA synthetase 1 (ACSL1). Therefore, we investigated the role of ACSL1 in the TNFα mediated production of GM-CSF. Our results showed that MDA-MB-231 cells displayed increased GM-CSF mRNA expression and secretion after incubation with TNFα. Blocking of ACSL1 activity in the cells with triacsin C markedly suppressed the secretion of GM-CSF. However, inhibition of β-oxidation and ceramide biosynthesis were not required for GM-CSF production. By small interfering RNA mediated knockdown, we further demonstrated that TNFα induced GM-CSF production was significantly diminished in ACSL1 deficient cells. TNFα mediated GM-CSF expression was significantly reduced by inhibition of p38 MAPK, ERK1/2 and NF-κB signaling pathways. TNFα induced phosphorylation of p38, ERK1/2, and NF-κB was observed during the secretion of GM-CSF. On the other hand, inhibition of ACSL1 activity attenuates TNFα mediated phosphorylation of p38 MAPK, ERK1/2, and NF-κB in the cells. Importantly, our findings suggest that ACSL1 plays an important role in the regulation of GM-CSF induced by TNFα in MDA-MB-231 cells. Therefore, ACSL1 may be considered as a potential novel therapeutic target for tumor growth.

Indexed as

Breast NeoplasmsCell Line, TumorCoenzyme A LigasesFemaleGene Knockout TechniquesGranulocyte-Macrophage Colony-Stimulating FactorHumansMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3NF-kappa Bp38 Mitogen-Activated Protein KinasesPhosphorylationSignal TransductionTriazenesTumor Necrosis Factor-alphaUp-RegulationACSL1 protein, humanCoenzyme A LigasesCSF2 protein, humanGranulocyte-Macrophage Colony-Stimulating FactorMAPK1 protein, humanMAPK3 protein, humanMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3NF-kappa Bp38 Mitogen-Activated Protein KinasesTNF protein, humantriacsin CTriazenesTumor Necrosis Factor-alphaACSL1GM-CSFMDA-MB-231TNFα

Identifiers

PMID31581558
PMCPMC6843696
OpenAlexW2977911328

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.