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Roles of DSCC1 and GINS1 in gastric cancer

Gastric carcinoma is a common malignant tumor originating from gastric mucosal epithelium. However, role of DS-cell cycle-dependent protein 1 (DSCC1) and GINS1 in gastric carcinoma remains unclear. The gastric carcinoma datasets GSE79973 and GSE118916 were downloaded from gene expression omnibus. Mu...

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Autores principales: Hou, Shiyang, Zhang, Jie, Chi, Xiaoqian, Li, Xiaowei, Zhang, Qijun, Kang, Chunbo, Shan, Haifeng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Lippincott Williams & Wilkins 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10615490/
https://www.ncbi.nlm.nih.gov/pubmed/37904396
http://dx.doi.org/10.1097/MD.0000000000035681
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author Hou, Shiyang
Zhang, Jie
Chi, Xiaoqian
Li, Xiaowei
Zhang, Qijun
Kang, Chunbo
Shan, Haifeng
author_facet Hou, Shiyang
Zhang, Jie
Chi, Xiaoqian
Li, Xiaowei
Zhang, Qijun
Kang, Chunbo
Shan, Haifeng
author_sort Hou, Shiyang
collection PubMed
description Gastric carcinoma is a common malignant tumor originating from gastric mucosal epithelium. However, role of DS-cell cycle-dependent protein 1 (DSCC1) and GINS1 in gastric carcinoma remains unclear. The gastric carcinoma datasets GSE79973 and GSE118916 were downloaded from gene expression omnibus. Multiple datasets were merged and batched. Differentially expressed genes (DEGs) were screened and weighted gene co-expression network analysis was performed. Functional enrichment analysis, gene set enrichment analysis and immune infiltration analysis were performed. Construction and analysis of protein-protein interaction Network. Survival analysis and comparative toxicogenomics database were performed. A heat map of gene expression was drawn. Target Scan screen miRNAs regulating DEGs. Two thousand forty-four DEGs were identified. According to gene ontology analysis, in biological process, they were mainly enriched in cell migration, transforming growth factor β receptor signaling pathway, angiogenesis, and steroid metabolism process. In cellular component, they were mainly enriched in extracellular vesicles, basement membrane, endoplasmic reticulum lumen, and extracellular space. In molecular function, they focused on extracellular matrix structural components, protein binding, platelet-derived growth factor binding, and catalytic activity. In Kyoto encyclopedia of genes and genomes, they were mainly enriched in protein digestion and absorption, metabolic pathways, fatty acid degradation, Glycerophospholipid metabolism, ether lipid metabolism. Gene set enrichment analysis showed that DEGs were mainly enriched in transforming growth factor β receptor signaling pathway, steroid metabolism process, basement membrane, endoplasmic reticulum lumen, structural components of extracellular matrix, platelet-derived growth factor binding, Glycerophospholipid metabolism, ether lipid metabolism. The results of immune infiltration analysis showed that expression of T cell CD4 memory resting was lower in the samples of gastric cancer. The core genes (TRIP13, CHEK1, DSCC1, GINS1) are protective factors, their expression shows a downward trend with increase of risk score. Comparative toxicogenomics database analysis showed that TRIP13, CHEK1, DSCC1, GINS1 were related to gastric tumors, gastric diseases, tumors, inflammation, and necrosis. DSCC1 and GINS1 are highly expressed in gastric cancer. Higher expression levels of DSCC1 and GINS1, worse the prognosis.
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spelling pubmed-106154902023-10-31 Roles of DSCC1 and GINS1 in gastric cancer Hou, Shiyang Zhang, Jie Chi, Xiaoqian Li, Xiaowei Zhang, Qijun Kang, Chunbo Shan, Haifeng Medicine (Baltimore) 5700 Gastric carcinoma is a common malignant tumor originating from gastric mucosal epithelium. However, role of DS-cell cycle-dependent protein 1 (DSCC1) and GINS1 in gastric carcinoma remains unclear. The gastric carcinoma datasets GSE79973 and GSE118916 were downloaded from gene expression omnibus. Multiple datasets were merged and batched. Differentially expressed genes (DEGs) were screened and weighted gene co-expression network analysis was performed. Functional enrichment analysis, gene set enrichment analysis and immune infiltration analysis were performed. Construction and analysis of protein-protein interaction Network. Survival analysis and comparative toxicogenomics database were performed. A heat map of gene expression was drawn. Target Scan screen miRNAs regulating DEGs. Two thousand forty-four DEGs were identified. According to gene ontology analysis, in biological process, they were mainly enriched in cell migration, transforming growth factor β receptor signaling pathway, angiogenesis, and steroid metabolism process. In cellular component, they were mainly enriched in extracellular vesicles, basement membrane, endoplasmic reticulum lumen, and extracellular space. In molecular function, they focused on extracellular matrix structural components, protein binding, platelet-derived growth factor binding, and catalytic activity. In Kyoto encyclopedia of genes and genomes, they were mainly enriched in protein digestion and absorption, metabolic pathways, fatty acid degradation, Glycerophospholipid metabolism, ether lipid metabolism. Gene set enrichment analysis showed that DEGs were mainly enriched in transforming growth factor β receptor signaling pathway, steroid metabolism process, basement membrane, endoplasmic reticulum lumen, structural components of extracellular matrix, platelet-derived growth factor binding, Glycerophospholipid metabolism, ether lipid metabolism. The results of immune infiltration analysis showed that expression of T cell CD4 memory resting was lower in the samples of gastric cancer. The core genes (TRIP13, CHEK1, DSCC1, GINS1) are protective factors, their expression shows a downward trend with increase of risk score. Comparative toxicogenomics database analysis showed that TRIP13, CHEK1, DSCC1, GINS1 were related to gastric tumors, gastric diseases, tumors, inflammation, and necrosis. DSCC1 and GINS1 are highly expressed in gastric cancer. Higher expression levels of DSCC1 and GINS1, worse the prognosis. Lippincott Williams & Wilkins 2023-10-27 /pmc/articles/PMC10615490/ /pubmed/37904396 http://dx.doi.org/10.1097/MD.0000000000035681 Text en Copyright © 2023 the Author(s). Published by Wolters Kluwer Health, Inc. https://creativecommons.org/licenses/by-nc/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial License 4.0 (CCBY-NC) (https://creativecommons.org/licenses/by-nc/4.0/) , where it is permissible to download, share, remix, transform, and buildup the work provided it is properly cited. The work cannot be used commercially without permission from the journal.
spellingShingle 5700
Hou, Shiyang
Zhang, Jie
Chi, Xiaoqian
Li, Xiaowei
Zhang, Qijun
Kang, Chunbo
Shan, Haifeng
Roles of DSCC1 and GINS1 in gastric cancer
title Roles of DSCC1 and GINS1 in gastric cancer
title_full Roles of DSCC1 and GINS1 in gastric cancer
title_fullStr Roles of DSCC1 and GINS1 in gastric cancer
title_full_unstemmed Roles of DSCC1 and GINS1 in gastric cancer
title_short Roles of DSCC1 and GINS1 in gastric cancer
title_sort roles of dscc1 and gins1 in gastric cancer
topic 5700
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10615490/
https://www.ncbi.nlm.nih.gov/pubmed/37904396
http://dx.doi.org/10.1097/MD.0000000000035681
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