Evidence map›Paper›PMID 40468330›Full record

ArticleCancer cell international2025

Disruption of DMD gene leads to altered calcium homeostasis and metabolic shift impacting gastric Cancer cell proliferation and migration.

Xiaodong Zou, Tong Wu, Tao Su, Hui Xiao, Chuyan Ni, Lijuan Hu, Wenchu Lin, Weilin Chen, Richard D Ye, Jianjiao Lin and 1 more

Abstract read
In one paragraph

Article in Cancer cell international, 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

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

2 citing papers in PubMed.

  1. Article
  2. Article
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.

Xiaodong ZouDepartment of Gastroenterology, The Second Affiliated Hospital, School of Medicine, The Chinese University of Hong Kong, Shenzhen & Longgang District People's Hospital of Shenzhen, Shenzhen, 518172, China.
Tong WuKobilka Institute of Innovative Drug Discovery, School of Medicine, The Chinese University of Hong Kong, Shenzhen, Guangdong, China.
Tao SuDepartment of Gastroenterology, The Second Affiliated Hospital, School of Medicine, The Chinese University of Hong Kong, Shenzhen & Longgang District People's Hospital of Shenzhen, Shenzhen, 518172, China.
Hui XiaoDepartment of Pathology, The Second Affiliated Hospital, School of Medicine, The Chinese University of Hong Kong, Shenzhen & Longgang District People's Hospital of Shenzhen, Shenzhen, 518172, China.
Chuyan NiDepartment of Gastroenterology, The Second Affiliated Hospital, School of Medicine, The Chinese University of Hong Kong, Shenzhen & Longgang District People's Hospital of Shenzhen, Shenzhen, 518172, China.
Lijuan HuDepartment of Gastroenterology, The Second Affiliated Hospital, School of Medicine, The Chinese University of Hong Kong, Shenzhen & Longgang District People's Hospital of Shenzhen, Shenzhen, 518172, China.
Wenchu LinInstitute of Digestive Disease, The Second Affiliated Hospital, School of Medicine, The Chinese University of Hong Kong, Shenzhen & Longgang District People's Hospital of Shenzhen, Shenzhen, 518172, China.
Weilin ChenMarshall Laboratory of Biomedical Engineering, Institute of Biological Therapy, Shenzhen University Medical School, Shenzhen University, Shenzhen, 518055, China.
Richard D YeKobilka Institute of Innovative Drug Discovery, School of Medicine, The Chinese University of Hong Kong, Shenzhen, Guangdong, China.
Jianjiao LinDepartment of Gastroenterology, The Second Affiliated Hospital, School of Medicine, The Chinese University of Hong Kong, Shenzhen & Longgang District People's Hospital of Shenzhen, Shenzhen, 518172, China. linjeana@126.com.
Li XiangDepartment of Gastroenterology, The Second Affiliated Hospital, School of Medicine, The Chinese University of Hong Kong, Shenzhen & Longgang District People's Hospital of Shenzhen, Shenzhen, 518172, China. shellyxiangli@163.com.

Funding

China Postdoctoral Science Foundation 2022M722184Joint Research Fund of the Second Affiliated Hospital-School of Medicine, The Chinese University of Hong Kong, Shenzhen YXLH17Joint Research Fund of the Second Affiliated Hospital-School of Medicine, The Chinese University of Hong Kong, Shenzhen YXLH2209Sanming Project of Medicine in Shenzen Municipality SZSM202105017Shenzhen Longgang District Science and Technology Innovation Commission Fund LGKCYLWS2021000012Shenzhen Science and Technology Innovation Commission Fund JCYJ20210324135005013Shenzhen Science and Technology Innovation Commission Fund JCYJ20230807141800001
6 · The paper itself

Abstract

backgroundDMD gene has been implicated in the progression and development of several tumors, but its specific contribution to gastric cancer (GC) has not been fully elucidated.

methodsWe validated DMD gene expression levels in the TIMER2.0 database and human gastric cancer tissue microarrays and constructed gastric precancerous lesion mouse models and DMD gene knockout and overexpression cell lines to investigate the role of DMD gene in gastric cancer development.

resultsIn this study, we found that DMD gene is significantly downregulated in GC cells and tissues. Mechanistic analysis revealed that DMD gene deletion increased intracellular calcium levels, disrupted mitochondrial homeostasis, and promoted a metabolic shift towards glycolysis, impacting GC cell proliferation and migration.

conclusionsTaken together, our results shed light on the novel role of DMD gene in gastric cancer development and provide valuable insights into potential therapeutic strategies.

Indexed as

Calcium homeostasisDMD geneGastric cancerGlycolysisMitochondrial dysfunction

Identifiers

PMID40468330
PMCPMC12139337

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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.