Abstract
Gastrointestinal stromal tumor (GIST) is the most common mesenchymal tumor in the gastrointestinal tracts and a model for the targeted therapy of solid tumors because of the oncogenic driver mutations in KIT and PDGDRA genes, which could be effectively inhibited by the very first targeted agent, imatinib mesylate. Most of the GIST patients could benefit a lot from the targeted treatment of this receptor tyrosine kinase inhibitor. However, more than 50% of the patients developed resistance within 2 years after imatinib administration, limiting the long-term effect of imatinib. Noncoding RNAs (ncRNAs), the non-protein coding transcripts of human, were demonstrated to play pivotal roles in the resistance of various chemotherapy drugs. In this review, we summarized the mechanisms of how ncRNAs functioning on the drug resistance in GIST. During the drug resistance of GIST, there were five regulating mechanisms where the functions of ncRNAs concentrated: oxidative phosphorylation, autophagy, apoptosis, drug target changes, and some signaling pathways. Also, these effects of ncRNAs in drug resistance were divided into two aspects. How ncRNAs regulate drug resistance in GIST was further summarized according to ncRNA types, different drugs and categories of resistance. Moreover, clinical applications of these ncRNAs in GIST chemotherapies concentrated on the prognostic biomarkers and novel therapeutic targets.
Highlights
Gastrointestinal stromal tumors (GISTs), the most common mesenchymal tumor in the gastrointestinal (GI) tracts, are malignancies generated from the interstitial cells of Cajal (ICCs) or their undifferentiated precursors (Sircar et al, 1999; Min and Leabu, 2006)
LncRNA CCDC26 knocking down decreased the apoptosis of GIST cells treated with imatinib through upregulating insulinlike growth factor 1 receptor (IGF-1R), which acted in the apoptosis pathways (Li et al, 2018; Yan et al, 2019b; Zhang Y. et al, 2019)
LncRNA CCDC26 knocking down decreased the apoptosis of GIST cells treated with imatinib through upregulating IGF-1R, which acted in the apoptosis pathways (Li et al, 2018; Yan et al, 2019b; Zhang Y. et al, 2019)
Summary
Reviewed by: Xiujuan Lei, Shaanxi Normal University, China Erik Wiemer, Erasmus University Medical Center, Netherlands Yebo Shao, Fudan University, China. We summarized the mechanisms of how ncRNAs functioning on the drug resistance in GIST. During the drug resistance of GIST, there were five regulating mechanisms where the functions of ncRNAs concentrated: oxidative phosphorylation, autophagy, apoptosis, drug target changes, and some signaling pathways. These effects of ncRNAs in drug resistance were divided into two aspects. How ncRNAs regulate drug resistance in GIST was further summarized according to ncRNA types, different drugs and categories of resistance. Clinical applications of these ncRNAs in GIST chemotherapies concentrated on the prognostic biomarkers and novel therapeutic targets
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
