{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Jin W"],"funding":["Science Research Foundation of Inner Mongolia People's Hospital","Science and Technology Planning Project for Health of Inner Mongolia","National Natural Science Foundation of China","Natural Science Foundation of Inner Mongolia Autonomous Region"],"pagination":["e70014"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11972004"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["19(1)"],"pubmed_abstract":["MicroRNAs (miRNAs) are crucial factors in gene regulation, and their dysregulation plays important roles in the immunity of gastric cancer (GC). However, finding specific and effective miRNA markers is still a great challenge for GC immunotherapy. In this study, we computed and analysed miRNA-seq, RNA-seq and clinical data of GC patients from the TCGA database. With the comparison of tumour and normal tissues in GC, we identified 2056 upregulated and 2311 downregulated protein-coding genes. Based on the miRNet database, more than 2600 miRNAs interact with these genes. Several key miRNAs, including hsa-mir-34a, hsa-mir-182 and hsa-mir-23b, were identified to potentially play important regulatory roles in the expression of most upregulated and downregulated genes in GC. Based on bioinformation approaches, the expressions of hsa-mir-34a and hsa-mir-182 were closely linked to the tumour stage, and high expression of hsa-mir-23b was correlated with poor survival in GC. Moreover, these three miRNAs are involved in immune cell infiltration (such as activated memory CD4 T cells and resting mast cells), particularly hsa-mir-182 and hsa-mir-23b. GSEA suggested that the changes in their expression may possibly activate/inhibit immune-related signal pathways, such as chemokine signalling pathway and CXCR4 pathway. These results will provide possible miRNA markers or targets for combined immunotherapy of GC."],"journal":["IET systems biology"],"pubmed_title":["Transcriptome Analyses Reveal the Important miRNAs Involved in Immune Response of Gastric Cancer."],"pmcid":["PMC11972004"],"funding_grant_id":["62171241","81960449","202202024","62262049","2021YN18","2022QN06007"],"pubmed_authors":["Cao L","Jin W","Liu J","Yang J","Yu L","Feng Z","Zuo Y","Wu C","Yang T"],"additional_accession":[]},"is_claimable":false,"name":"Transcriptome Analyses Reveal the Important miRNAs Involved in Immune Response of Gastric Cancer.","description":"MicroRNAs (miRNAs) are crucial factors in gene regulation, and their dysregulation plays important roles in the immunity of gastric cancer (GC). However, finding specific and effective miRNA markers is still a great challenge for GC immunotherapy. In this study, we computed and analysed miRNA-seq, RNA-seq and clinical data of GC patients from the TCGA database. With the comparison of tumour and normal tissues in GC, we identified 2056 upregulated and 2311 downregulated protein-coding genes. Based on the miRNet database, more than 2600 miRNAs interact with these genes. Several key miRNAs, including hsa-mir-34a, hsa-mir-182 and hsa-mir-23b, were identified to potentially play important regulatory roles in the expression of most upregulated and downregulated genes in GC. Based on bioinformation approaches, the expressions of hsa-mir-34a and hsa-mir-182 were closely linked to the tumour stage, and high expression of hsa-mir-23b was correlated with poor survival in GC. Moreover, these three miRNAs are involved in immune cell infiltration (such as activated memory CD4 T cells and resting mast cells), particularly hsa-mir-182 and hsa-mir-23b. GSEA suggested that the changes in their expression may possibly activate/inhibit immune-related signal pathways, such as chemokine signalling pathway and CXCR4 pathway. These results will provide possible miRNA markers or targets for combined immunotherapy of GC.","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Jan-Dec","modification":"2025-07-08T03:13:52.739Z","creation":"2025-07-08T03:13:52.739Z"},"accession":"S-EPMC11972004","cross_references":{"pubmed":["40186852"],"doi":["10.1049/syb2.70014"]}}