Evidence map›Paper›PMID 37316264›Full record

ArticleJournal for immunotherapy of cancer2023

2,5-dimethylcelecoxib alleviated NK and T-cell exhaustion in hepatocellular carcinoma via the gastrointestinal microbiota-AMPK-mTOR axis.

Banglun Pan, Zhanfei Chen, Xiaoxia Zhang, Zengbin Wang, Yuxin Yao, Xiaoxuan Wu, Jiacheng Qiu, Hua Lin, Liumin Yu, Haijian Tu and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal for immunotherapy of cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

28 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
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  6. The Immune Microenvironment in Liver Cancer: From Analysis to Targeting.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
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  18. Article
  19. Frontiers in pharmacology · 2025
    Article
  20. Celecoxib in oncology: targeting the COX-2/PGEFrontiers in pharmacology · 2025
    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

11 authors at 2 institutions in 1 country.

Banglun Pan *Department of Hepatobiliary Surgery and Fujian Institute of Hepatobiliary Surgery, Fujian Medical University Union Hospital, Fuzhou, China.
Zhanfei Chen *Department of Laboratory Medicine, Affiliated Hospital of Putian University, Putian, China.
Xiaoxia ZhangDepartment of Hepatobiliary Surgery and Fujian Institute of Hepatobiliary Surgery, Fujian Medical University Union Hospital, Fuzhou, China.
Zengbin WangDepartment of Hepatobiliary Surgery and Fujian Institute of Hepatobiliary Surgery, Fujian Medical University Union Hospital, Fuzhou, China.
Yuxin YaoDepartment of Hepatobiliary Surgery and Fujian Institute of Hepatobiliary Surgery, Fujian Medical University Union Hospital, Fuzhou, China.
Xiaoxuan WuDepartment of Hepatobiliary Surgery and Fujian Institute of Hepatobiliary Surgery, Fujian Medical University Union Hospital, Fuzhou, China.
Jiacheng QiuDepartment of Hepatobiliary Surgery and Fujian Institute of Hepatobiliary Surgery, Fujian Medical University Union Hospital, Fuzhou, China.
Hua LinDepartment of Laboratory Medicine, Affiliated Hospital of Putian University, Putian, China.
Liumin YuDepartment of Laboratory Medicine, Affiliated Hospital of Putian University, Putian, China.
Haijian TuSchool of Basic Medical Sciences, Putian University, Putian, China.
Nanhong TangDepartment of Hepatobiliary Surgery and Fujian Institute of Hepatobiliary Surgery, Fujian Medical University Union Hospital, Fuzhou, China fztnh@fjmu.edu.cn.ORCID 0000-0001-7495-5254
Fujian Medical University · CNPutian University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background2,5-dimethylcelecoxib (DMC), a derivative of celecoxib, is an inhibitor of microsomal prostaglandin E synthase-1 (mPGES-1). Our previous studies have demonstrated that DMC inhibits the expression of programmed death-ligand 1 on hepatocellular carcinoma (HCC) cells to prevent tumor progression. However, the effect and mechanism of DMC on HCC infiltrating immune cells remain unclear.

methodsIn this study, single-cell-based high-dimensional mass cytometry was performed on the tumor microenvironment of HCC mice treated with DMC, celecoxib and MK-886 (a known mPGES-1 inhibitor). Moreover, 16S ribosomal RNA sequencing was employed to analyze how DMC improved the tumor microenvironment of HCC by remodeling the gastrointestinal microflora.

resultsWe found that (1) DMC significantly inhibited the growth of HCC and improved the prognosis of the mice, and this depended on the stronger antitumor activity of natural killer (NK) and T cells; (2) compared with celecoxib and MK-886, DMC significantly enhanced the cytotoxic and stem-like potential, and inhibited exhaustion of NK and T cells; (3) mechanistically, DMC inhibited the expression of programmed cell death protein-1 and upregulated interferon-γ expression of NK and T cells via the gastrointestinal microbiota (Bacteroides acidifaciens, Odoribacter laneus, and Odoribacter splanchnicus)-AMPK-mTOR axis.

conclusionsOur study uncovers the role of DMC in improving the tumor microenvironment of HCC, which not only enriches the relationship between the mPGES-1/prostaglandin E2 pathway and the antitumor function of NK and T cells, but also provide an important strategic reference for multitarget or combined immunotherapy of HCC.Cite Now.

Indexed as

Carcinoma, HepatocellularGastrointestinal MicrobiomeLiver NeoplasmsAMP-Activated Protein KinasesAnimalsCelecoxibChlorobenzenesDinoprostoneIndolesMicePyrazolesSulfonamidesT-Cell ExhaustionTumor Microenvironment2,5-dimethylcelecoxibAMP-Activated Protein KinasesCelecoxibChlorobenzenesDinoprostoneIndolesMK-886PyrazolesSulfonamidesCD8-Positive T-LymphocytesInflammation MediatorsLiver NeoplasmsLymphocytes, Tumor-InfiltratingTumor Microenvironment

Identifiers

PMID37316264
PMCPMC10277542
OpenAlexW4380685859

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.