The Potential CircRNAs in Imatinib Resistance of GIST

preprint OA: closed CC-BY-4.0
🔓 Open OA copy View at publisher

Abstract

Background: Recent studies have found that circular RNA is an abundant RNA species, belongs to part of the competing endogenous RNA network(ceRNA), which was proved to play an important role in the development, diagnosis and progress of diseases. Methods: : We determined the expression of circular RNAs in paired normal gastric tissues(N), primary GIST (gastrointestinal stromal tumor) tissues (Y or YC) and imatinib mesylate secondary resistance GIST tissues(C) with microarray and predicted 8677 dysregulated circular RNAs. Results: : We identified 15 circRNAs was up-regulated and 8 circRNAs were down-regulated in C group. Gene ontology (GO)and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis indicated that these host linear transcripts that differentially express circular RNAs are involved in many key biological pathways., predicting the potential tumor-genesis and drug resistance mechanism was related with HIF-1 pathway, later we draw the cirRNA-miRNA-mRNA network involved in the HIF-1 pathway, found that several dysregulated circRNAs and the relationship between circRNA-miRNAs-mRNA, such as circRNA_06551, circRNA_14668, circRNA_04497, circRNA_08683, circRNA_09923(Green, down-regulation) and circRNA_23636, circRNA_15734(Red, up-regulation). Conclusions: : Taken together, we identified a panel of dysregulated circRNAs that may be potential biomarkers even therapy relevant to the GIST, especially imatinib secondary resistance GIST.

My notes (saved in your browser only)

Citation neighborhood (no data yet)

We don't have any in-corpus citations linked to this paper yet. The paper's references may be in our DB but unresolved to ``paper_id`` (resolution happens at ingest when the cited DOI matches a row we already have). Run the cross-source citation reconcile pass to retry.

Source provenance

europepmc
last seen: 2026-05-19T01:45:01.086888+00:00
unpaywall
last seen: 2026-05-28T02:00:01.590549+00:00
License: CC-BY-4.0