Evidence map›Paper›PMID 30218403›Full record

ArticleCellular and molecular neurobiology2018

The Beta-Hydroxybutyrate Suppresses the Migration of Glioma Cells by Inhibition of NLRP3 Inflammasome.

Sen Shang, Leilei Wang, Yali Zhang, Haixia Lu, Xiaoyun Lu

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

43 citing papers in PubMed, 71 citations in OpenAlex.

  1. Review
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  3. Review
  4. Review
  5. Frontiers in neurology · 2026
    Article
  6. Article
  7. Review
  8. Article
  9. Article
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  11. Review
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  14. Review
  15. Article
  16. Article
  17. New Insights on NLRP3 Inflammasome: Mechanisms of Activation, Inhibition, and Epigenetic Regulation.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024
    Review
  18. Review
  19. Review
  20. Article
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.

Sen ShangKey Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, 710049, Shaanxi, People's Republic of China.
Leilei WangKey Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, 710049, Shaanxi, People's Republic of China.
Yali ZhangKey Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, 710049, Shaanxi, People's Republic of China.
Haixia LuKey Laboratory of Environment and Genes Related to Diseases of Ministry of Education, Institute of Neurobiology, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Centre, Xi'an, 710061, Shaanxi, People's Republic of China. hxl01@xjtu.edu.cn.
Xiaoyun LuKey Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, 710049, Shaanxi, People's Republic of China. luxy05@xjtu.edu.cn.ORCID http://orcid.org/0000-0003-3284-4729
Xi'an Jiaotong University · CN

Funding

National Natural Science Foundation of China 81172170National Natural Science Foundation of China 81371288
6 · The paper itself

Abstract

Activation of inflammasome leads to the formation of an inflammatory microenvironment which plays an important role in the process of cancer development. Beta-hydroxybutyrate (BHB) is a ketone body that has recently been reported to exert anti-inflammatory effects via inhibition of NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome. Here, we investigated the potential influence of BHB on the in vitro migration of C6 glioma cells and the activation of NLRP3 inflammasome. Our results indicated that administration of BHB suppressed C6 cells migration and NLRP3 inflammasome activation, reducing the levels of activated cysteinyl aspartate-specific proteinase 1 (caspase-1) and mature Interleukin 1β (IL-1β). Fully activation of NLRP3 inflammasome was induced by lipopolysaccharide (LPS) prime plus adenosine triphosphate (ATP) stimulation in C6 cells, which promoted in vitro migration of C6 cell. BHB also counteracted the LPS/ATP-promoted cell migration by suppressing the activation of caspase-1 and the maturation of IL-1β. The enhancement of phospho-signal transducer and activator of transcription 3 (p-STAT3), degradation of nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IκBα) as well as the overexpression of fibroblast growth factor 2 (FGF2) resulting from LPS/ATP treatment, and subsequent IL-1β maturation could also be compensated by BHB. Our results suggested that BHB inhibits the activation of NLRP3 inflammasome in C6 glioma cells and consequently suppressed the C6 cell migration. These findings also implicated that by inhibiting NLRP3 inflammasome, BHB reduced the inflammatory microenvironment which provided ancillary therapeutic benefits for the intervention of glioma.

Indexed as

3-Hydroxybutyric AcidAdenosine TriphosphateAnimalsBrain NeoplasmsCell Line, TumorCell MovementCell SurvivalGliomaInflammasomesLipopolysaccharidesNLR Family, Pyrin Domain-Containing 3 ProteinPertussis ToxinRats3-Hydroxybutyric AcidAdenosine TriphosphateInflammasomesLipopolysaccharidesNLR Family, Pyrin Domain-Containing 3 ProteinPertussis ToxinBeta-hydroxybutyrateGliomaMigrationNLRP3 inflammasome

Identifiers

PMID30218403
PMCPMC11469911
OpenAlexW2891390124

What OpenQuestion holds

Textmetadata
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.