Abstract:       Gastrointestinal stromal tumor (GIST) is the most common gastrointestinal mesenchymal tumors, mainly due to the onset of the proto-oncogene receptor tyrosine kinase, or platelet-derived growth factor receptor gene activating mutations. Molecular targeted therapy drug of imatinib mesylate inhibit KIT, platelet-derived growth factor receptor aloha (PDGFRA) gene tyrosine kinase activity, which is effective in patients with advanced GIST. However, a growing number of studies have found the presence of imatinib mesylate in primary and secondary drug resistance in the treatment of GIST process. With the in-depth study of the physiological function and mechanism of action of noncoding RNA in recent years, making it gradually realized extensive regulation of non-coding RNA gene expression, which occurs in tumor development, invasion and metastasis, drug resistance and other processes plays an important role. Non-coding RNA has the potential to explore GIST pathogenesis and resistance mechanisms to provide new ideas and direction.

Key words: Gastrointestinal stromal tumor, Imatinib mesylate, Non-coding RNA