Qi Wang , Yifan Li , Xiaoqiang Niu , Chengjiang Zhang , Jun Zhang , Jiaqing Cao , Lidong Wu
{"title":"SNORD3A在胃癌中作为潜在的预后和治疗生物标志物","authors":"Qi Wang , Yifan Li , Xiaoqiang Niu , Chengjiang Zhang , Jun Zhang , Jiaqing Cao , Lidong Wu","doi":"10.1016/j.ejbt.2023.08.004","DOIUrl":null,"url":null,"abstract":"<div><h3>Background</h3><p>Although SNORD3A has been implicated in cancer progression, its specific roles and underlying mechanisms in gastric cancer (GC) remain poorly understood. We analysed SNORD3A expression using TCGA data and evaluated patient survival via Kaplan‒Meier curves. Additionally, we conducted GO-KEGG enrichment analysis to identify relevant biological processes and signaling pathways, while ssGSEA was used to assess the correlation between SNORD3A and cancer immune infiltrates. Furthermore, we explored the relationship between SNORD3A and immunotherapy response through TIDE. We verified SNORD3A expression using real-time qPCR and assessed cell proliferation, migration, and invasion via CCK8 and Transwell migration and invasion assays.</p></div><div><h3>Results</h3><p>Our results revealed that SNORD3A was significantly upregulated in GC, with high expression correlating with poor survival. SNORD3A and related genes were primarily enriched in the insulin/insulin-related growth factor signaling pathway. We also observed negative associations between SNORD3A expression and several immune cells, including activated dendritic cells, CD56bright natural killer cells, central memory CD8 T cells, effector memory CD8 T cells, effector memory CD4 T cells, eosinophils, immature dendritic cells, macrophages, mast cells, MDSCs, memory B cells, monocytes, neutrophil cells, plasmacytoid dendritic cells, regulatory T cells, and T follicular helper cells. High SNORD3A expression also correlated with a poorer response to immunotherapy. Finally, inhibition of SNORD3A suppressed cell proliferation, migration, and invasion.</p></div><div><h3>Conclusions</h3><p>Our findings suggest that SNORD3A plays a catalytic role in the proliferation, migration and invasiveness of GC and may have potential as a diagnostic biomarker and therapeutic target for GC.</p><p><strong>How to cite:</strong> Wang Q, Li Y, Niu X, et al. SNORD3A acts as a potential prognostic and therapeutic biomarker in gastric cancer. Electron J Biotechnol 2023; 67. <span>https://doi.org/10.1016/j.ejbt.2023.08.004</span><svg><path></path></svg>.</p></div>","PeriodicalId":11529,"journal":{"name":"Electronic Journal of Biotechnology","volume":"67 ","pages":"Pages 1-12"},"PeriodicalIF":2.3000,"publicationDate":"2023-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S071734582300026X/pdfft?md5=d76e7dba0ae8e127e2b08a4642d7e44a&pid=1-s2.0-S071734582300026X-main.pdf","citationCount":"0","resultStr":"{\"title\":\"SNORD3A acts as a potential prognostic and therapeutic biomarker in gastric cancer\",\"authors\":\"Qi Wang , Yifan Li , Xiaoqiang Niu , Chengjiang Zhang , Jun Zhang , Jiaqing Cao , Lidong Wu\",\"doi\":\"10.1016/j.ejbt.2023.08.004\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><h3>Background</h3><p>Although SNORD3A has been implicated in cancer progression, its specific roles and underlying mechanisms in gastric cancer (GC) remain poorly understood. We analysed SNORD3A expression using TCGA data and evaluated patient survival via Kaplan‒Meier curves. Additionally, we conducted GO-KEGG enrichment analysis to identify relevant biological processes and signaling pathways, while ssGSEA was used to assess the correlation between SNORD3A and cancer immune infiltrates. Furthermore, we explored the relationship between SNORD3A and immunotherapy response through TIDE. We verified SNORD3A expression using real-time qPCR and assessed cell proliferation, migration, and invasion via CCK8 and Transwell migration and invasion assays.</p></div><div><h3>Results</h3><p>Our results revealed that SNORD3A was significantly upregulated in GC, with high expression correlating with poor survival. SNORD3A and related genes were primarily enriched in the insulin/insulin-related growth factor signaling pathway. We also observed negative associations between SNORD3A expression and several immune cells, including activated dendritic cells, CD56bright natural killer cells, central memory CD8 T cells, effector memory CD8 T cells, effector memory CD4 T cells, eosinophils, immature dendritic cells, macrophages, mast cells, MDSCs, memory B cells, monocytes, neutrophil cells, plasmacytoid dendritic cells, regulatory T cells, and T follicular helper cells. High SNORD3A expression also correlated with a poorer response to immunotherapy. Finally, inhibition of SNORD3A suppressed cell proliferation, migration, and invasion.</p></div><div><h3>Conclusions</h3><p>Our findings suggest that SNORD3A plays a catalytic role in the proliferation, migration and invasiveness of GC and may have potential as a diagnostic biomarker and therapeutic target for GC.</p><p><strong>How to cite:</strong> Wang Q, Li Y, Niu X, et al. SNORD3A acts as a potential prognostic and therapeutic biomarker in gastric cancer. 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SNORD3A acts as a potential prognostic and therapeutic biomarker in gastric cancer
Background
Although SNORD3A has been implicated in cancer progression, its specific roles and underlying mechanisms in gastric cancer (GC) remain poorly understood. We analysed SNORD3A expression using TCGA data and evaluated patient survival via Kaplan‒Meier curves. Additionally, we conducted GO-KEGG enrichment analysis to identify relevant biological processes and signaling pathways, while ssGSEA was used to assess the correlation between SNORD3A and cancer immune infiltrates. Furthermore, we explored the relationship between SNORD3A and immunotherapy response through TIDE. We verified SNORD3A expression using real-time qPCR and assessed cell proliferation, migration, and invasion via CCK8 and Transwell migration and invasion assays.
Results
Our results revealed that SNORD3A was significantly upregulated in GC, with high expression correlating with poor survival. SNORD3A and related genes were primarily enriched in the insulin/insulin-related growth factor signaling pathway. We also observed negative associations between SNORD3A expression and several immune cells, including activated dendritic cells, CD56bright natural killer cells, central memory CD8 T cells, effector memory CD8 T cells, effector memory CD4 T cells, eosinophils, immature dendritic cells, macrophages, mast cells, MDSCs, memory B cells, monocytes, neutrophil cells, plasmacytoid dendritic cells, regulatory T cells, and T follicular helper cells. High SNORD3A expression also correlated with a poorer response to immunotherapy. Finally, inhibition of SNORD3A suppressed cell proliferation, migration, and invasion.
Conclusions
Our findings suggest that SNORD3A plays a catalytic role in the proliferation, migration and invasiveness of GC and may have potential as a diagnostic biomarker and therapeutic target for GC.
How to cite: Wang Q, Li Y, Niu X, et al. SNORD3A acts as a potential prognostic and therapeutic biomarker in gastric cancer. Electron J Biotechnol 2023; 67. https://doi.org/10.1016/j.ejbt.2023.08.004.
期刊介绍：
Electronic Journal of Biotechnology is an international scientific electronic journal, which publishes papers from all areas related to Biotechnology. It covers from molecular biology and the chemistry of biological processes to aquatic and earth environmental aspects, computational applications, policy and ethical issues directly related to Biotechnology.
The journal provides an effective way to publish research and review articles and short communications, video material, animation sequences and 3D are also accepted to support and enhance articles. The articles will be examined by a scientific committee and anonymous evaluators and published every two months in HTML and PDF formats (January 15th , March 15th, May 15th, July 15th, September 15th, November 15th).
The following areas are covered in the Journal:
• Animal Biotechnology
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• Biosafety
• Biotechnology Industry
• Biotechnology of Human Disorders
• Chemical Engineering
• Environmental Biotechnology
• Food Biotechnology
• Marine Biotechnology
• Microbial Biotechnology
• Molecular Biology and Genetics
•Nanobiotechnology
• Omics
• Plant Biotechnology
• Process Biotechnology
• Process Chemistry and Technology
• Tissue Engineering
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