Neoplasma Vol.65, No.5, p.683-692, 2018
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Title: Identification of critical microRNAs in gastrointestinal stromal tumor patients treated with Imatinib |
Author: Z. Zhang, N. y. Jiang, R. y. Guan, Y. k. Zhu, F. q. Jiang, D. Piao |
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Abstract: Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal neoplasms of the gastrointestinal tract. Imatinib mesylate was considered a breakthrough drug in clinical treatment of GIST, but GIST patients showed resistance to it. We aimed to identify critical microRNAs (miRNAs) related to imatinib resistance in imatinib-treated GIST patients. Microarray datasets under accession numbers GSE63159 and GSE45901 were downloaded from the Gene Expression Omnibus (GEO) database. The differentially expressed miRNAs (DEMs) related to imatinib resistance were identified. GO function and KEGG pathway enrichment analyses were performed, and lncRNA-miRNA-target gene regulatory networks were constructed. Finally, the critical miRNAs and their target genes related to imatinib resistance or sensitivity were identified. A total of 20 DEMs in the GSE63159 dataset (7 significantly up-regulated and 13 down-regulated) and 23 DEMs in the GSE45901 dataset (8 up-regulated and 15 down-regulated) were identified. Five critical miRNAs and 109 target genes were identified in the lncRNA-miRNA-target gene regulatory networks. GO function and KEGG pathway enrichment analysis showed that DEM target genes were mainly involved in several signaling pathways, such as focal adhesion and the GnRH signaling pathway. From the five miRNAs, the overexpression of hsa-miR-28-5p and hsa-miR-125a-5p had significant correlation to imatinib resistance or imatinib sensitivity in GIST patients. In addition, Hsa-miR-28-5p and hsa-miR-125a-5p may be involved in the development and progression of GIST, and they may serve as prognostic markers for imatinib-response in GIST patients.
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Keywords: gastrointestinal stromal tumors; microRNAs; imatinib mesylate; RNA, long noncoding; focal adhesions; gonadotropin-releasing hormone |
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Published online: 24-Sep-2018
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Year: 2018, Volume: 65, Issue: 5 |
Page From: 683, Page To: 692 |
doi:10.4149/neo_2018_170906N575
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