顺铂
骨肉瘤
细胞凋亡
癌症研究
长非编码RNA
细胞生物学
分子生物学
生物
核糖核酸
化学
化疗
生物化学
基因
遗传学
作者
Yuan Wang,Li Zhang,Xifu Zheng,Weiliang Zhong,Xiliang Tian,Baosheng Yin,Kui Tian,Weiguo Zhang
出处
期刊:Cancer Letters
[Elsevier]
日期:2016-11-01
卷期号:382 (2): 137-146
被引量:120
标识
DOI:10.1016/j.canlet.2016.08.024
摘要
Chemotherapeutic insensitivity remains a major obstacle to osteosarcoma treatment. Recently, increasing evidence has suggested that long non-coding RNAs (lncRNAs) play an essential role in tumourigenesis. However, the potential biological roles and regulatory mechanisms of novel lncRNAs in response to cisplatin treatment are poorly understood. Here, we found that lncRNA LINC00161 was induced by cisplatin in osteosarcoma cells. Elevated LINC00161 increased cisplatin-induced apoptosis and reversed the cisplatin-resistant phenotype of osteosarcoma cells by upregulating IFIT2. Further mechanistic studies revealed that LINC00161 could sponge endogenous miR-645 and inhibit its activity leading to IFIT2 increase. In addition, we identified that LINC00161 enhanced cisplatin-induced apoptosis through regulation of the miR-645-IFIT2 pathway. Thus, these findings demonstrate that LINC00161 is an essential regulator in cisplatin-induced apoptosis, and the LINC00161-miR-645-IFIT2 signalling axis plays an important role in reducing osteosarcoma chemoresistance.
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