Evidence map›Paper›PMID 40087771›Full record

ArticleBiomarker research2025

NLRP4 unlocks an NK/macrophages-centered ecosystem to suppress non-small cell lung cancer.

Zhouwenli Meng, Jian Li, Hui Wang, Zhengqi Cao, Wenqing Lu, Xiaomin Niu, Yi Yang, Ziming Li, Ying Wang, Shun Lu

Abstract read
In one paragraph

Article in Biomarker research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
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.

Zhouwenli Meng *Shanghai Lung Cancer Center, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, P. R. China.
Jian Li *Shanghai Lung Cancer Center, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, P. R. China.
Hui Wang *Shanghai Lung Cancer Center, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, P. R. China.
Zhengqi CaoShanghai Lung Cancer Center, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, P. R. China.
Wenqing LuShanghai Lung Cancer Center, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, P. R. China.
Xiaomin NiuShanghai Lung Cancer Center, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, P. R. China.
Yi YangShanghai Lung Cancer Center, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, P. R. China.
Ziming LiShanghai Lung Cancer Center, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, P. R. China. liziming1980@shsmu.edu.cn.
Ying WangShanghai Institute of Immunology, Department of Immunology and Microbiology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, P. R. China. ywangssmu@shsmu.edu.cn.
Shun LuShanghai Lung Cancer Center, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, P. R. China. shunlu@sjtu.edu.cn.

Funding

National Natural Science Foundation of China 82030045National Natural Science Foundation of China 82072564National Natural Science Foundation of China 82241228Shanghai Pujiang Program 21PJD065
6 · The paper itself

Abstract

backgroundTumor immune evasion extends beyond T cells, affecting innate immune elements like natural killer cells (NK) and macrophages within the tumor-immune microenvironment (TIME). Nevertheless, translational strategies to trigger collaboration of NK cells and macrophages to initiate sufficient anti-tumor cytoxicity remain scarce and are urgently needed.

methodsIn this study, TCGA datasets was used to confirm the prognosis value of the expression level of NLR family pyrin domain containing 4 (NLRP4) in NSCLC and the tumor tissues microarray was used to further check its clinical-relevance at protein-level. Subsequently, a tumor cell line with stable NLRP4 overexpression was established and subcutaneous tumor models in C57BL/6J mice were used to validate the anti-tumor characteristics of NLRP4. After analyzing the tumor microenvironment using flow cytometry and multiplex immunofluorescence, we further validated our findings through co-culture transwell assays and TCGA analysis. Utilizing bulk-RNA sequencing, proteomics, and mass spectrometry of mouse tumor tissues, we innovatively identified the downstream pathways of NLRP4 and verified them through co-immunoprecipitation (co-IP) and Western blot (WB) experiments.

resultsNLRP4 could trigger a distinct anti-tumor ecosystem organized by TIGIT

conclusionAltogether, we delineated NLRP4's unexplored facets and discovered an NLRP4-driven anti-tumor ecosystem composed of TIGIT

Indexed as

ChemokinesMacrophagesNatural killer cellNLRP4PP2A

Identifiers

PMID40087771
PMCPMC11909883

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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.