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pmid:35726219
Integrated Bioinformatics Analysis for Identifying the Significant Genes as Poor Prognostic Markers in Gastric Adenocarcinoma.
Yamei Li · Yan Luo · Qiang Tian · Yu Lai · Lei Xu · Hailong Yun · Yang Liang · Dandan Liao · Rui Gu · Liye Liu · Mu Yuan · Yijiao Li · Yufan Li · Mingze Lu · Xin Yong · Hua Zhang
Journal of oncology · 2022 doi:10.1155/2022/9080460
Paper
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Experiment
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Data
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Analysis
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Execution
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Complete file
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The purpose of this study was to identify significant genes and key pathways participated in the initiation and progression of GAC. Four datasets (GSE13911, GSE19826, GSE54129, and GSE79973) including 171 GAC and 77 normal tissues from Gene Expression Omnibus (GEO) database were collected and analyzed. Through integrated bioinformatics analysis, we obtained 69 commonly differentially expressed genes (DEGs) among the four datasets, including 20 upregulated and 49 downregulated genes. The prime module in protein-protein interaction network of DEGs, including ADAMTS2, COL10A1, COL1A1, COL1A2, COL8A1, BGN, and SPP1, was enriched in protein digestion and absorption, ECM-receptor interaction, focal adhesion, PI3K-Akt signaling pathway, and amoebiasis. Furthermore, expression and survival analysis found that all seven hub genes were highly expressed in GAC tissues and 6 of them (except for SPP1) were able to predict poor prognosis of GAC. Finally, we verified the 6 high-expressed hub genes in GAC tissues via immunohistochemistry, Western blot, and RNA quantification analysis. Altogether, we identified six significantly upregulated DEGs as poor prognostic markers in GAC based on integrated bioinformatical methods, which could be potential molecular markers and therapeutic targets for GAC patients.", "claims": [{"id": "claim-method", "statement": "The GEO2R online tools [18] were used to identify DEGs between the GAC specimen and normal specimen with |log2FC| > 2 and an adjusted P value <0.05 [16–18].", "kind": "methodological", "target": null, "evidence": [{"asset": "source:pmid:35726219", "locator": "sections[4] \"2.2. 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