| Literature DB >> 27117758 |
Le Qu1, Jin Ding2, Cheng Chen3, Zhen-Jie Wu1, Bing Liu1, Yi Gao1, Wei Chen1, Feng Liu4, Wen Sun2, Xiao-Feng Li2, Xue Wang2, Yue Wang5, Zhen-Yu Xu5, Li Gao6, Qing Yang7, Bin Xu7, Yao-Ming Li7, Zi-Yu Fang7, Zhi-Peng Xu1, Yi Bao1, Deng-Shuang Wu1, Xiong Miao8, Hai-Yang Sun9, Ying-Hao Sun7, Hong-Yang Wang10, Lin-Hui Wang11.
Abstract
Sunitinib resistance is a major challenge for advanced renal cell carcinoma (RCC). Understanding the underlying mechanisms and developing effective strategies against sunitinib resistance are highly desired in the clinic. Here we identified an lncRNA, named lncARSR (lncRNA Activated in RCC with Sunitinib Resistance), which correlated with clinically poor sunitinib response. lncARSR promoted sunitinib resistance via competitively binding miR-34/miR-449 to facilitate AXL and c-MET expression in RCC cells. Furthermore, bioactive lncARSR could be incorporated into exosomes and transmitted to sensitive cells, thus disseminating sunitinib resistance. Treatment of sunitinib-resistant RCC with locked nucleic acids targeting lncARSR or an AXL/c-MET inhibitor restored sunitinib response. Therefore, lncARSR may serve as a predictor and a potential therapeutic target for sunitinib resistance.Entities:
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Year: 2016 PMID： 27117758 DOI： 10.1016/j.ccell.2016.03.004
Source DB: PubMed Journal: Cancer Cell ISSN： 1535-6108 Impact factor: 31.743