Evidence map›Paper›PMID 33613529›Full record

ArticleFrontiers in immunology2020

Therapeutic Potential of Pharmacological Targeting NLRP3 Inflammasome Complex in Cancer.

Gulcin Tezcan, Ekaterina E Garanina, Mohammad Alsaadi, Zarema E Gilazieva, Ekaterina V Martinova, Maria I Markelova, Svetlana S Arkhipova, Shaimaa Hamza, Alan McIntyre, Albert A Rizvanov and 1 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 10% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.

  1. Pooled it
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  5. IL-18-Mediated Tumor Immune Evasion.Current issues in molecular biology · 2026
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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

11 authors at 3 institutions in 4 countries.

Gulcin TezcanInstitute of Fundamental Medicine and Biology, Kazan Federal University, Kazan, Russia.
Ekaterina E GaraninaInstitute of Fundamental Medicine and Biology, Kazan Federal University, Kazan, Russia.
Mohammad AlsaadiInstitute of Fundamental Medicine and Biology, Kazan Federal University, Kazan, Russia.
Zarema E GilazievaInstitute of Fundamental Medicine and Biology, Kazan Federal University, Kazan, Russia.
Ekaterina V MartinovaInstitute of Fundamental Medicine and Biology, Kazan Federal University, Kazan, Russia.
Maria I MarkelovaInstitute of Fundamental Medicine and Biology, Kazan Federal University, Kazan, Russia.
Svetlana S ArkhipovaInstitute of Fundamental Medicine and Biology, Kazan Federal University, Kazan, Russia.
Shaimaa HamzaInstitute of Fundamental Medicine and Biology, Kazan Federal University, Kazan, Russia.
Alan McIntyreCentre for Cancer Sciences, Faculty of Medicine and Health Sciences, University of Nottingham, Nottingham, United Kingdom.
Albert A RizvanovInstitute of Fundamental Medicine and Biology, Kazan Federal University, Kazan, Russia.
Svetlana F KhaiboullinaInstitute of Fundamental Medicine and Biology, Kazan Federal University, Kazan, Russia.
Kazan Federal University · RUBursa Uludağ Üni̇versi̇tesi̇ · TRUniversity of Nottingham · GB

Funding

Medical Research Council MR/P010334/1
6 · The paper itself

Abstract

Introduction: Dysregulation of NLRP3 inflammasome complex formation can promote chronic inflammation by increased release of IL-1β. However, the effect of NLRP3 complex formation on tumor progression remains controversial. Therefore, we sought to determine the effect of NLRP3 modulation on the growth of the different types of cancer cells, derived from lung, breast, and prostate cancers as well as neuroblastoma and glioblastoma Method: The effect of Caspase 1 inhibitor (VX765) and combination of LPS/Nigericin on NLRP3 inflammasome activity was analyzed in A549 (lung cancer), MCF-7 (breast cancer), PC3 (prostate cancer), SH-SY5Y (neuroblastoma), and U138MG (glioblastoma) cells. Human fibroblasts were used as control cells. The effect of VX765 and LPS/Nigericin on NLRP3 expression was analyzed using western blot, while IL-1β and IL-18 secretion was detected by ELISA. Tumor cell viability and progression were determined using Annexin V, cell proliferation assay, LDH assay, sphere formation assay, transmission electron microscopy, and a multiplex cytokine assay. Also, angiogenesis was investigated by a tube formation assay. VEGF and MMPs secretion were detected by ELISA and a multiplex assay, respectively. Statistical analysis was done using one-way ANOVA with Tukey's analyses and Kruskal-Wallis one-way analysis of variance. Results: LPS/Nigericin increased NRLP3 protein expression as well as IL-1β and IL-18 secretion in PC3 and U138MG cells compared to A549, MCF7, SH-SY5Y cells, and fibroblasts. In contrast, MIF expression was commonly found upregulated in A549, PC3, SH-SY5Y, and U138MG cells and fibroblasts after Nigericin treatment. Nigericin and a combination of LPS/Nigericin decreased the cell viability and proliferation. Also, LPS/Nigericin significantly increased tumorsphere size in PC3 and U138MG cells. In contrast, the sphere size was reduced in MCF7 and SH-SY5Y cells treated with LPS/Nigericin, while no effect was detected in A549 cells. VX765 increased secretion of CCL24 in A549, MCF7, PC3, and fibroblasts as well as CCL11 and CCL26 in SH-SY5Y cells. Also, VX765 significantly increased the production of VEGF and MMPs and stimulated angiogenesis in all tumor cell lines. Discussion: Our data suggest that NLRP3 activation using Nigericin could be a novel therapeutic approach to control the growth of tumors producing a low level of IL-1β and IL-18.

Indexed as

A549 CellsAntineoplastic AgentsCell ProliferationCell SurvivalCytokinesDipeptidesHumansInflammasomesInflammation MediatorsMCF-7 CellsMitochondriaMolecular Targeted TherapyNeoplasmsNeovascularization, PathologicNigericinNLR Family, Pyrin Domain-Containing 3 ProteinAntineoplastic AgentsbelnacasanCytokinesDipeptidesInflammasomesInflammation MediatorsNigericinNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanpara-AminobenzoatescancerIL-1βinflammasomenigericinNLRP3

Identifiers

PMID33613529
PMCPMC7887322
OpenAlexW3128616509

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.