Evidence map›Paper›PMID 39020183›Full record

ArticleDigestive diseases and sciences2024

Regulation of the PD-1/PD-L1 Axis and NK Cell Dysfunction by Exosomal miR-552-5p in Gastric Cancer.

Chun-Wei Tang, Jin-Hua Yang, Jing-Wen Qin, Hui-Jie Wu, Hao-Peng Cui, Lian-Ying Ge, Ai-Qun Liu

Abstract read
In one paragraph

Article in Digestive diseases and sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

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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

14 citing papers in PubMed.

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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

7 authors.

Chun-Wei Tang *Department of Endoscopy, Guangxi Medical University Cancer Hospital, Nanning, 530021, Guangxi, China.
Jin-Hua Yang *Department of Endoscopy, Guangxi Medical University Cancer Hospital, Nanning, 530021, Guangxi, China.
Jing-Wen QinDepartment of Endoscopy, Guangxi Medical University Cancer Hospital, Nanning, 530021, Guangxi, China.
Hui-Jie WuDepartment of Digestive Endoscopy Center, Fujian Provincial Hospital, Fuzhou, 350001, Fujian, China.
Hao-Peng CuiDepartment of Endoscopy, Guangxi Medical University Cancer Hospital, Nanning, 530021, Guangxi, China.
Lian-Ying GeDepartment of Endoscopy, Guangxi Medical University Cancer Hospital, Nanning, 530021, Guangxi, China.
Ai-Qun LiuDepartment of Endoscopy, Guangxi Medical University Cancer Hospital, Nanning, 530021, Guangxi, China. liuaiqun2004@163.com.

Funding

Funding for the development and promotion of suitable medical and health technologies in Guangxi S2022107Guangxi Key Research and Development Program AB18221084Guangxi Key Research and Development Program AB20297021National Natural Scientific Foundation of China 82360559Regional High-Incidence Diseases Research of Guangxi Natural Science Foundation under Grant 2023GXNSFAA026298
6 · The paper itself

Abstract

objectiveNK cells play a vital role in tumor immune resistance. Various factors affect NK cell activity. While NK cell dysfunction has been observed in numerous malignancies, the underlying mechanisms in gastric cancer remain unclear.

methodFlow cytometry was used to identify the phenotypic distribution and expression of activated receptors on NK cells. ELISA was used to determine the expression of cytokines. We examined the expression of NK cell-related genes and explored their association with survival and prognosis. Additionally, we conducted PCR detection of miR-552-5p expression levels in plasma exosomes of patients and investigated its correlation with phenotypic distribution and activated receptors. We used flow cytometry and ELISA to verify the role of miR-552-5p in NK cell dysfunction. Furthermore, we investigated the potential role of PD-1/PD-L1 in regulating NK cell dysfunction in patients' cells.

resultsWe observed a significant decrease in the percentage of NKG2D and NKp30 and IFN-γ and TNF-α in patients than in healthy volunteers. Patients with low levels of CD56, CD16, NKG2D, and NKP46 exhibited poorer survival prognoses. Moreover, increased expression levels of plasma exosomal miR-552-5p in patients were negatively associated with NK cell phenotypic distribution and activated receptor expression. MiR-552-5p downregulated the secretion of perforin, granzyme, and IFN-γ as well as the expression of NKp30, NKp46, and NKG2D. Additionally, it suppressed the cytotoxicity of NK cells. The inhibitory effect of miR-552-5p, on NK cell function was reversed when anti-PD-L1 antibodies were used.

conclusionExosomal miR-552-5p targets the PD-1/PD-L1 axis, leading to impaired NK cell function.

Indexed as

B7-H1 AntigenExosomesKiller Cells, NaturalMicroRNAsProgrammed Cell Death 1 ReceptorStomach NeoplasmsAgedCase-Control StudiesCD56 AntigenFemaleGene Expression Regulation, NeoplasticHumansInterferon-gammaMaleMiddle AgedNatural Cytotoxicity Triggering Receptor 1B7-H1 AntigenCD274 protein, humanCD56 AntigenInterferon-gammaKLRK1 protein, humanMicroRNAsMIRN552 microRNA, humanNatural Cytotoxicity Triggering Receptor 1Natural Cytotoxicity Triggering Receptor 3NCR1 protein, humanNCR3 protein, humanNK Cell Lectin-Like Receptor Subfamily KPDCD1 protein, humanProgrammed Cell Death 1 ReceptorReceptors, IgGTumor Necrosis Factor-alphaDysfunctionExosomeGastric cancermiR-552-5pNatural killer cell

Identifiers

PMID39020183
PMCPMC11415408

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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.