Evidence map›Paper›PMID 39060229›Full record

ArticleCell death & disease2024

PPAR-γ/NF-kB/AQP3 axis in M2 macrophage orchestrates lung adenocarcinoma progression by upregulating IL-6.

Guofu Lin, Lanlan Lin, Xiaohui Chen, Luyang Chen, Jiansheng Yang, Yanling Chen, Danwen Qian, Yiming Zeng, Yuan Xu

Abstract read
In one paragraph

Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing 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

27 citing papers in PubMed.

  1. Review
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  15. Aquaporins: a novel perspective in the treatment of lung diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
  16. Review
  17. Ethanolic Extract ofPharmaceuticals (Basel, Switzerland) · 2025
    Article
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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

9 authors.

Guofu Lin *Fujian Provincial Clinical Research Center of Interventional Respirology, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian Province, 362000, China.
Lanlan Lin *Fujian Provincial Clinical Research Center of Interventional Respirology, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian Province, 362000, China.
Xiaohui ChenFujian Provincial Clinical Research Center of Interventional Respirology, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian Province, 362000, China.
Luyang ChenFujian Provincial Clinical Research Center of Interventional Respirology, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian Province, 362000, China.
Jiansheng YangDepartment of Thoracic Surgery, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian province, 362000, China.
Yanling ChenClinical Research Center, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian Province, 362000, China.
Danwen QianThe Tumor Immunogenomics and Immunosurveillance (TIGI) Lab, UCL Cancer Institute, London, UK.
Yiming ZengFujian Provincial Clinical Research Center of Interventional Respirology, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian Province, 362000, China. zeng_yiming@fjmu.edu.cn.
Yuan XuFujian Provincial Clinical Research Center of Interventional Respirology, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian Province, 362000, China. yuan_xu0123@fjmu.edu.cn.ORCID 0000-0002-3694-2871

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82203208Natural Science Foundation of Fujian Province (Fujian Provincial Natural Science Foundation) 2021J01254
6 · The paper itself

Abstract

Aquaporin 3 (AQP3), which is mostly expressed in pulmonary epithelial cells, was linked to lung adenocarcinoma (LUAD). However, the underlying functions and mechanisms of AQP3 in the tumor microenvironment (TME) of LUAD have not been elucidated. Single-cell RNA sequencing (scRNA-seq) was used to study the composition, lineage, and functional states of TME-infiltrating immune cells and discover AQP3-expressing subpopulations in five LUAD patients. Then the identifications of its function on TME were examined in vitro and in vivo. AQP3 was associated with TNM stages and lymph node metastasis of LUAD patients. We classified inter- and intra-tumor diversity of LUAD into twelve subpopulations using scRNA-seq analyses. The analysis showed AQP3 was mainly enriched in subpopulations of M2 macrophages. Importantly, mechanistic investigations indicated that AQP3 promoted M2 macrophage polarization by the PPAR-γ/NF-κB axis, which affected tumor growth and migration via modulating IL-6 production. Mixed subcutaneous transplanted tumor mice and Aqp3 knockout mice models were further utilized, and revealed that AQP3 played a critical role in mediating M2 macrophage polarization, modulating glucose metabolism in tumors, and regulating both upstream and downstream pathways. Overall, our study demonstrated that AQP3 could regulate the proliferation, migration, and glycometabolism of tumor cells by modulating M2 macrophages polarization through the PPAR-γ/NF-κB axis and IL-6/IL-6R signaling pathway, providing new insight into the early detection and potential therapeutic target of LUAD.

Indexed as

Adenocarcinoma of LungAquaporin 3Interleukin-6Lung NeoplasmsMacrophagesNF-kappa BPPAR gammaAnimalsCell Line, TumorDisease ProgressionFemaleHumansMaleMiceMice, Inbred C57BLMice, KnockoutAQP3 protein, humanAquaporin 3Interleukin-6NF-kappa BPPAR gamma

Identifiers

PMID39060229
PMCPMC11282095

What OpenQuestion holds

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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.