Evidence map›Paper›PMID 35216164›Full record

ArticleInternational journal of molecular sciences2022

Association of Tim-3/Gal-9 Axis with NLRC4 Inflammasome in Glioma Malignancy: Tim-3/Gal-9 Induce the NLRC4 Inflammasome.

JeongMin Sim, JeongMan Park, Suwan Kim, Sojung Hwang, KyoungSu Sung, Jung-Eun Lee, SeungHo Yang, Kyunggi Cho, SungHwan Lee, Jong-Seok Moon and 2 more

Abstract read
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In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
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

18 citing papers in PubMed.

  1. Review
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  15. Dysregulation of inflammasome activation in glioma.Cell communication and signaling : CCS · 2023
    Review
  16. Article
  17. Non-canonical NLRC4 inflammasomes in astrocytes contribute to glioma malignancy.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Article
  18. 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

12 authors.

JeongMin SimDepartment of Neurosurgery, Bundang CHA Medical Center, CHA University, Seongnam 13496, Korea.
JeongMan ParkDepartment of Neurosurgery, Bundang CHA Medical Center, CHA University, Seongnam 13496, Korea.ORCID 0000-0003-2849-4594
Suwan KimDepartment of Neurosurgery, Bundang CHA Medical Center, CHA University, Seongnam 13496, Korea.
Sojung HwangDepartment of Neurosurgery, Bundang CHA Medical Center, CHA University, Seongnam 13496, Korea.
KyoungSu SungDepartment of Neurosurgery, Dong-A University Hospital, Dong-A University College of Medicine, Busan 49201, Korea.
Jung-Eun LeeDepartment of Neurosurgery, St. Vincent's Hospital, College of Medicine, The Catholic University of Korea, Seoul 16247, Korea.
SeungHo YangDepartment of Neurosurgery, St. Vincent's Hospital, College of Medicine, The Catholic University of Korea, Seoul 16247, Korea.ORCID 0000-0002-3490-1064
Kyunggi ChoDepartment of Neurosurgery, Bundang CHA Medical Center, CHA University, Seongnam 13496, Korea.
SungHwan LeeDepartment of Surgery, Bundang CHA Medical Center, CHA University, Seongnam 13496, Korea.ORCID 0000-0003-3365-0096
Jong-Seok MoonSoonchunhyang Institution of Medi-Bio Science (SIMS), Soonchunhyang University, Cheonan-si 31151, Korea.ORCID 0000-0002-2537-7854
JuWon AhnDepartment of Neurosurgery, Bundang CHA Medical Center, CHA University, Seongnam 13496, Korea.
Jaejoon LimDepartment of Neurosurgery, Bundang CHA Medical Center, CHA University, Seongnam 13496, Korea.ORCID 0000-0001-8299-8078

Funding

Ministry of Science, Technology and Information Grant No. 2021R1F1A105780111Ministry of Trade, Industry and Energy Grant No. 10067378
6 · The paper itself

Abstract

Tim-3/Gal-9 and the NLRC4 inflammasome contribute to glioma progression. However, the underlying mechanisms involved are unclear. Here, we observed that Tim-3/Gal-9 expression increased with glioma malignancy and found that Tim-3/Gal-9 regulate NLRC4 inflammasome formation and activation. Tim-3/Gal-9 and NLRC4 inflammasome-related molecule expression levels increased with WHO glioma grade, and this association was correlated with low survival. We investigated NLRC4 inflammasome formation by genetically regulating Tim-3 and its ligand Gal-9. Tim-3/Gal-9 regulation was positively correlated with the NLRC4 inflammasome, NLRC4, and caspase-1 expression. Tim-3/Gal-9 did not trigger IL-1β secretion but were strongly positively correlated with caspase-1 activity as they induced programmed cell death in glioma cells. A protein-protein interaction analysis revealed that the FYN-JAK1-ZNF384 pathways are bridges in NLRC4 inflammasome regulation by Tim-3/Gal-9. The present study showed that Tim-3/Gal-9 are associated with poor prognosis in glioma patients and induce NLRC4 inflammasome formation and activation. We proposed that a Tim-3/Gal-9 blockade could be beneficial in glioma therapy as it would reduce the inflammatory microenvironment by downregulating the NLRC4 inflammasome.

Indexed as

Brain NeoplasmsCalcium-Binding ProteinsCARD Signaling Adaptor ProteinsCaspase 1Cell Line, TumorGalectinsGliomaHepatitis A Virus Cellular Receptor 2HumansInflammasomesJanus Kinase 1Protein BindingTrans-ActivatorsCalcium-Binding ProteinsCARD Signaling Adaptor ProteinsCaspase 1GalectinsHAVCR2 protein, humanHepatitis A Virus Cellular Receptor 2InflammasomesJAK1 protein, humanJanus Kinase 1LGALS9 protein, humanNLRC4 protein, humanTrans-ActivatorsZNF384 protein, humangliomaglioma malignancyNLRC4 inflammasomeTim-3/Gal-9

Identifiers

PMID35216164
PMCPMC8878774

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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.