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Prediction of Novel Biomarkers for Gastric Intestinal Metaplasia and Gastric Adenocarcinoma Using Bioinformatics Analysis Publisher



Eskandarion MR1 ; Eskandarieh S2 ; Shakoori Farahani A3 ; Mahmoodzadeh H4 ; Shahi F5 ; Oghabian MA6 ; Shirkoohi R1
Authors
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Authors Affiliations
  1. 1. Cancer Research Center, Cancer Institute, IKHC, Tehran University of Medical Sciences, Tehran, Iran
  2. 2. Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran
  3. 3. Medical Genetics Ward, IKHC Hospital Complex, Tehran University of Medical Sciences, Tehran, Iran
  4. 4. Department of Surgery, Cancer Research Center, Cancer Institute, IKHC, Tehran University of Medical Sciences, Tehran, Iran
  5. 5. Department of Medical Oncology, Cancer Research Center, Cancer Institute, IKHC, Tehran University of Medical Sciences, Tehran, Iran
  6. 6. Medical Physics Department, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran

Source: Heliyon Published:2024


Abstract

Background & aim: The histologic and molecular changes from intestinal metaplasia (IM) to gastric cancer (GC) have not been fully characterized. The present study sought to identify potential alterations in signaling pathways in IM and GC to predict disease progression; these alterations can be considered therapeutic targets. Materials & methods: Seven gene expression profiles were selected from the GEO database. Discriminate differentially expressed genes (DEGs) were analyzed by EnrichR. The STRING database, Cytoscape, Gene Expression Profiling Interactive Analysis (GEPIA), cBioPortal, NetworkAnalyst, MirWalk database, OncomiR, and bipartite miRNA‒mRNA correlation network was used for downstream analyses of selected module genes. Results: Analyses revealed that extracellular matrix-receptor interactions (ITGB1, COL1A1, COL1A2, COL4A1, FN1, COL6A3, and THBS2) in GC and PPAR signaling pathway interactions (FABP1, APOC3, APOA1, HMGCS2, and PPARA and PCK1) in IM may play key roles in both the carcinogenesis and progression of underlying GC from intestinal metaplasia. IM enrichment indicated that this is closely related to digestion and absorption. The TF-hub gene regulatory network revealed that AR, TCF4, SALL4, and ESR1 were more important for hub gene expression. It was revealed that the development and prediction of GC may be affected by hsa-miR-29. It was found that PTGR1, C1orf115, CRYL1, ALDOB, and SULT1B1 were downregulated in GC and upregulated in IM. Therefore, they might have tumor suppressor activity in GC progression. Conclusion: New potential biomarkers and pathways involved in GC and IM were identified that are important for the transformation of GC from IM to adenocarcinoma and can be therapeutic targets for GC. © 2024
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