Evidence map›Paper›PMID 40775351›Full record

ArticleJournal of translational medicine2025

Calcium overload via PVT1 reprograms neutrophil fate and constrains gastric cancer progression.

Dong Wang, Yunlong Li, Xiaoyu Peng, Lulu Zhang, Ying Zhang, Xue Guan, Xiao Liang, Songbin Fu, Jingcui Yu

Abstract read
In one paragraph

Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

Who cites it

2 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

9 authors.

Dong Wang *Scientific Research Centre, the Second Affiliated Hospital of Harbin Medical University, Harbin, 150081, China.
Yunlong Li *Department of General Surgery, the Second Affiliated Hospital of Harbin Medical University, Harbin, 150081, China.
Xiaoyu PengScientific Research Centre, the Second Affiliated Hospital of Harbin Medical University, Harbin, 150081, China.
Lulu ZhangScientific Research Centre, the Second Affiliated Hospital of Harbin Medical University, Harbin, 150081, China.
Ying ZhangMinistry of Education, Key Laboratory of Preservation of Human Genetic Resources and Disease Control in China (Harbin Medical University), Harbin, 150081, China.
Xue GuanAnimal Laboratory Center, the Second Affiliated Hospital of Harbin Medical University, Harbin, 150081, China.
Xiao LiangMinistry of Education, Key Laboratory of Preservation of Human Genetic Resources and Disease Control in China (Harbin Medical University), Harbin, 150081, China.
Songbin FuMinistry of Education, Key Laboratory of Preservation of Human Genetic Resources and Disease Control in China (Harbin Medical University), Harbin, 150081, China.
Jingcui YuScientific Research Centre, the Second Affiliated Hospital of Harbin Medical University, Harbin, 150081, China. yujingcui@ems.hrbmu.edu.cn.ORCID 0000-0002-1936-4379

Funding

the Innovative Scientific Research Fund of Harbin Medical University 31041210020the Open Project Program of Key Laboratory of Preservation of Human Genetic Resources and Disease Control in China (Harbin Medical University), Ministry of Education LPHGRD2022-007
6 · The paper itself

Abstract

backgroundThe aberrant upregulation of PVT1 in gastric cancer (GC) has emerged as a critical molecular marker, while its mechanism of remodeling the tumor microenvironment (TME) through metabolic regulation remains unclear. This study aims to unveil the novel mechanism by which PVT1 regulates the fate determination of tumor-associated neutrophils (TANs) via the calcium signaling pathway.

methodsClinical analysis of 90 GC cases revealed a correlation between PVT1 expression and neutrophil infiltration in tumor tissues. Mechanistically, multi-omics integration of transcriptomics and 4D-label-free quantitative proteomics identified PVT1-associated pathways driving GC progression. Functional validation through in vitro and in vivo models demonstrated PVT1's oncogenic role, while transcriptomic profiling further decoded neutrophil activation mechanisms regulated by PVT1.

resultsThe expression of PVT1 was significantly elevated in GC tissues compared to adjacent non-tumor tissues (p < 0.001), with 73.3% of cases showing an increased proportion of PVT1-positive cells. High PVT1 expression negatively correlated with the infiltration of neutrophils (r = - 0.3554, p = 0.0012), and patients in the PVT1 + CD66b- subgroup exhibited the poorest prognosis, characterized by a median survival of 20.5 months and a mortality rate of 72.5%. Silencing PVT1 upregulated calcium signaling pathway-related genes (RYR2 and RYR3) in GC cells, accompanied by a marked increase in intracellular Ca

conclusionsOverall, this study provides the first evidence that PVT1 establishes a metabolic checkpoint by inducing calcium overload, thereby regulating both the senescence process and functional phenotype of neutrophils, which provides a novel metabolic intervention target for GC immunotherapy.

Indexed as

CalciumDisease ProgressionNeutrophilsRNA, Long NoncodingStomach NeoplasmsAnimalsCalcium SignalingCell Line, TumorCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansMaleMice, NudeMiddle AgedTumor MicroenvironmentCalciumPVT1 long-non-coding RNA, humanRNA, Long NoncodingCalcium signaling pathwayGastric cancerPVT1Replicative senescenceTumor-associated neutrophils

Identifiers

PMID40775351
PMCPMC12330090

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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.