中国癌症杂志 ›› 2015, Vol. 25 ›› Issue (5): 392-396.doi: 10.3969/j.issn.1007-3969.2015.05.013

• 综述 • 上一篇    下一篇

非编码RNA在胃肠间质瘤中的研究进展

王春萌,陈杰,师英强   

  1. 复旦大学附属肿瘤医院胃及软组织外科,复旦大学上海医学院肿瘤学系,上海 200032
  • 出版日期:2015-05-30 发布日期:2015-08-11
  • 通信作者: 师英强 E-mail:yingqiangshi@126.com

Research progress of non-coding RNA in gastrointestinal stromal tumor

WANG Chunmeng, CHEN Jie, SHI Yingqiang   

  1. Department of Gastric Cancer and Soft Tissue Sarcomas, Fudan University Shanghai Cancer Center; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China)
  • Published:2015-05-30 Online:2015-08-11
  • Contact: SHI Yingqiang E-mail: yingqiangshi@126.com

摘要:    胃肠间质瘤(gastrointestinal stromal tumor,GIST)是消化道最常见的间叶源性肿瘤,发病原因主要是由于原癌基因受体酪氨酸激酶或血小板衍生生长因子受体基因活化突变。分子靶向治疗药物甲磺酸伊马替尼是抑制KIT、血小板衍生生长因子受体α多肽(platelet-derived growth factor receptor alpha,PDGFRA)基因酪氨酸激酶活性的药物,其能有效治疗进展期GIST。但是,越来越多的研究发现,甲磺酸伊马替尼在治疗GIST过程中存在原发性耐药和继发性耐药。随着近年来对非编码RNA的生理功能和作用机制的深入研究,使人们逐步认识到非编码RNA对基因表达的广泛调控作用,其在肿瘤发生、发展、侵袭、转移和耐药等过程中扮演着重要角色。研究非编码RNA有可能为探讨GIST发病及耐药机制提供新的思路和方向。

关键词: 胃肠间质瘤, 甲磺酸伊马替尼, 非编码RNA

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