DMD基因的破坏导致钙稳态改变和代谢转变，影响胃癌细胞的增殖和迁移。
Disruption of DMD gene leads to altered calcium homeostasis and metabolic shift impacting gastric Cancer cell proliferation and migration.
作者信息
Zou Xiaodong, Wu Tong, Su Tao, Xiao Hui, Ni Chuyan, Hu Lijuan, Lin Wenchu, Chen Weilin, Ye Richard D, Lin Jianjiao, Xiang Li
机构信息
Department 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.
Guangdong Key Laboratory for Biomedical Measurements and Ultrasound Imaging, National-Regional Key Technology Engineering Laboratory for Medical Ultrasound, School of Biomedical Engineering, Shenzhen University Medical School, Shenzhen, 518060, China.
出版信息
Cancer Cell Int. 2025 Jun 4;25(1):202. doi: 10.1186/s12935-025-03829-4.
BACKGROUND
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.
METHODS
We validated gene expression levels in the TIMER2.0 database and human gastric cancer tissue microarrays and constructed gastric precancerous lesion mouse models and gene knockout and overexpression cell lines to investigate the role of gene in gastric cancer development.
RESULTS
In this study, we found that gene is significantly downregulated in GC cells and tissues. Mechanistic analysis revealed that gene deletion increased intracellular calcium levels, disrupted mitochondrial homeostasis, and promoted a metabolic shift towards glycolysis, impacting GC cell proliferation and migration.
CONCLUSIONS
Taken together, our results shed light on the novel role of gene in gastric cancer development and provide valuable insights into potential therapeutic strategies.
SUPPLEMENTARY INFORMATION
The online version contains supplementary material available at 10.1186/s12935-025-03829-4.
背景
基因已被证明与多种肿瘤的进展和发展有关，但其对胃癌（GC）的具体作用尚未完全阐明。
方法
我们在TIMER2.0数据库和人胃癌组织微阵列中验证了基因表达水平，并构建了胃癌前病变小鼠模型以及基因敲除和过表达细胞系，以研究基因在胃癌发展中的作用。
结果
在本研究中，我们发现基因在GC细胞和组织中显著下调。机制分析表明，基因缺失会增加细胞内钙水平，破坏线粒体稳态，并促进向糖酵解的代谢转变，影响GC细胞的增殖和迁移。
结论
综上所述，我们的结果揭示了基因在胃癌发展中的新作用，并为潜在的治疗策略提供了有价值的见解。
补充信息
在线版本包含可在10.1186/s12935-025-03829-4获取的补充材料。
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