Evidence map›Paper›PMID 40185713›Full record

ArticleCell death & disease2025

A small molecule directly targets NLRP3 to promote inflammasome activation and antitumor immunity.

Xuemei Liu, Hongbin He, Minghui Qi, Zhongjun Jiang, Bolong Lin, Xiaqiong Wang, Di Wang, Ming Ma, Wei Jiang, Rongbin Zhou

Abstract read
In one paragraph

Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. The Roles of ProteinCancer communications (London, England) · 2026
    Review
  8. Review
  9. Modulators of the Human Voltage-Gated Proton Channel HPharmaceuticals (Basel, Switzerland) · 2025
    Review
  10. 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

10 authors.

Xuemei LiuNational Key Laboratory of immune response and immunotherapy, Center for Advanced Interdisciplinary Science and Biomedicine of IHM, School of Basic Medical Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, China.
Hongbin HeNational Key Laboratory of immune response and immunotherapy, Center for Advanced Interdisciplinary Science and Biomedicine of IHM, School of Basic Medical Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, China.
Minghui QiNational Key Laboratory of immune response and immunotherapy, Center for Advanced Interdisciplinary Science and Biomedicine of IHM, School of Basic Medical Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, China.
Zhongjun JiangNational Key Laboratory of immune response and immunotherapy, Center for Advanced Interdisciplinary Science and Biomedicine of IHM, School of Basic Medical Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, China.
Bolong LinNational Key Laboratory of immune response and immunotherapy, Center for Advanced Interdisciplinary Science and Biomedicine of IHM, School of Basic Medical Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, China.
Xiaqiong WangNational Key Laboratory of immune response and immunotherapy, Center for Advanced Interdisciplinary Science and Biomedicine of IHM, School of Basic Medical Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, China.
Di WangInstitute of Immunology, Zhejiang University School of Medicine, Hangzhou, China.ORCID http://orcid.org/0000-0002-2712-1705
Ming MaNational Key Laboratory of immune response and immunotherapy, Center for Advanced Interdisciplinary Science and Biomedicine of IHM, School of Basic Medical Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, China. mm685@ustc.edu.cn.ORCID http://orcid.org/0009-0007-2797-4410
Wei JiangNational Key Laboratory of immune response and immunotherapy, Center for Advanced Interdisciplinary Science and Biomedicine of IHM, School of Basic Medical Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, China. ustcjw@ustc.edu.cn.ORCID http://orcid.org/0000-0001-8327-3079
Rongbin ZhouNational Key Laboratory of immune response and immunotherapy, Center for Advanced Interdisciplinary Science and Biomedicine of IHM, School of Basic Medical Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, China. zrb1980@ustc.edu.cn.

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81821001National Natural Science Foundation of China (National Science Foundation of China) 82130107National Natural Science Foundation of China (National Science Foundation of China) 82371768National Natural Science Foundation of China (National Science Foundation of China) U20A20359
6 · The paper itself

Abstract

Immune checkpoint blockade (ICB) therapies have emerged as promising treatment of cancer, but the efficacy is limited. NLRP3 inflammasome activation in tumor microenvironment can promote the infiltration of cytotoxic lymphocytes and antitumor immunity, but it is unclear whether ICB resistance can be overcome by directly targeting NLRP3. Here we show that a small molecule compound directly targeting NLRP3 can induce inflammasome activation and anti-tumor immunity. 2-guanidinobezimidazole (2GBI) directly bound to NLRP3 and induced inflammasome activation, which was independent of potassium efflux, chloride efflux and mitochondrial dysfunction. 2GBI treatment alone promoted anti-tumor immunity and inhibited tumor growth via NLRP3-dependent manner. Moreover, 2GBI treatment could overcome ICB resistance and exerted synergistic anti-tumor effects. These results suggest that targeting NLRP3 is a potential strategy to induce anti-tumor immunity and improve the efficacy of ICB.

Indexed as

InflammasomesNeoplasmsNLR Family, Pyrin Domain-Containing 3 ProteinAnimalsCell Line, TumorHumansMiceMice, Inbred C57BLTumor MicroenvironmentInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanNlrp3 protein, mouse

Identifiers

PMID40185713
PMCPMC11971322

What OpenQuestion holds

Textmetadata
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.