Exosome-Transmitted lncARSR Promotes Sunitinib Resistance in Renal Cancer by Acting as a Competing Endogenous RNA
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 Suni...
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| Published in | Cancer cell Vol. 29; no. 5; pp. 653 - 668 |
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| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
09.05.2016
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| Subjects | |
| Online Access | Get full text |
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| 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.
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•lncARSR promotes sunitinib resistance and predicts poor response of RCC patients•Intercellular transfer of lncARSR by exosomes disseminates sunitinib resistance•lncARSR acts as a ceRNA for miR-34 and miR-449 to promote AXL and c-MET expression•Targeting lncARSR or AXL/c-MET in sunitinib-resistant RCC restores drug sensitivity
Qu et al. identify lncARSR as a mediator of sunitinib resistance in renal cell carcinoma by acting as a competing endogenous RNA for miR-34 and miR-449, thereby increasing expression of their targets AXL and c-MET, and show that exosome-mediated transmission of lncARSR can confer resistance to sensitive cells. |
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| AbstractList | 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.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. 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. 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. [Display omitted] •lncARSR promotes sunitinib resistance and predicts poor response of RCC patients•Intercellular transfer of lncARSR by exosomes disseminates sunitinib resistance•lncARSR acts as a ceRNA for miR-34 and miR-449 to promote AXL and c-MET expression•Targeting lncARSR or AXL/c-MET in sunitinib-resistant RCC restores drug sensitivity Qu et al. identify lncARSR as a mediator of sunitinib resistance in renal cell carcinoma by acting as a competing endogenous RNA for miR-34 and miR-449, thereby increasing expression of their targets AXL and c-MET, and show that exosome-mediated transmission of lncARSR can confer resistance to sensitive cells. |
| Author | Sun, Hai-Yang Wu, Zhen-Jie Bao, Yi Gao, Yi Li, Yao-Ming Sun, Wen Liu, Bing Xu, Zhi-Peng Li, Xiao-Feng Chen, Cheng Gao, Li Liu, Feng Fang, Zi-Yu Yang, Qing Xu, Zhen-Yu Wang, Hong-Yang Ding, Jin Miao, Xiong Qu, Le Chen, Wei Xu, Bin Wang, Xue Wang, Yue Wang, Lin-Hui Wu, Deng-Shuang Sun, Ying-Hao |
| Author_xml | – sequence: 1 givenname: Le surname: Qu fullname: Qu, Le organization: Department of Urology, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China – sequence: 2 givenname: Jin surname: Ding fullname: Ding, Jin organization: The International Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Hospital, Second Military Medical University, Shanghai 200433, China – sequence: 3 givenname: Cheng surname: Chen fullname: Chen, Cheng organization: The International Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Hospital, Second Military Medical University, Shanghai 200433, China – sequence: 4 givenname: Zhen-Jie surname: Wu fullname: Wu, Zhen-Jie organization: Department of Urology, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China – sequence: 5 givenname: Bing surname: Liu fullname: Liu, Bing organization: Department of Urology, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China – sequence: 6 givenname: Yi surname: Gao fullname: Gao, Yi organization: Department of Urology, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China – sequence: 7 givenname: Wei surname: Chen fullname: Chen, Wei organization: Department of Urology, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China – sequence: 8 givenname: Feng surname: Liu fullname: Liu, Feng organization: Department of Medical Genetics, College of Basic Medicine, Second Military Medical University, Shanghai 200433, China – sequence: 9 givenname: Wen surname: Sun fullname: Sun, Wen organization: The International Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Hospital, Second Military Medical University, Shanghai 200433, China – sequence: 10 givenname: Xiao-Feng surname: Li fullname: Li, Xiao-Feng organization: The International Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Hospital, Second Military Medical University, Shanghai 200433, China – sequence: 11 givenname: Xue surname: Wang fullname: Wang, Xue organization: The International Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Hospital, Second Military Medical University, Shanghai 200433, China – sequence: 12 givenname: Yue surname: Wang fullname: Wang, Yue organization: Department of Histology and Embryology, College of Basic Medicine, Second Military Medical University, Shanghai 200433, China – sequence: 13 givenname: Zhen-Yu surname: Xu fullname: Xu, Zhen-Yu organization: Department of Histology and Embryology, College of Basic Medicine, Second Military Medical University, Shanghai 200433, China – sequence: 14 givenname: Li surname: Gao fullname: Gao, Li organization: Department of Pathology, Changhai Hospital, Second Military Medical University, Shanghai 200433, China – sequence: 15 givenname: Qing surname: Yang fullname: Yang, Qing organization: Department of Urology, Changhai Hospital, Second Military Medical University, Shanghai 200433, China – sequence: 16 givenname: Bin surname: Xu fullname: Xu, Bin organization: Department of Urology, Changhai Hospital, Second Military Medical University, Shanghai 200433, China – sequence: 17 givenname: Yao-Ming surname: Li fullname: Li, Yao-Ming organization: Department of Urology, Changhai Hospital, Second Military Medical University, Shanghai 200433, China – sequence: 18 givenname: Zi-Yu surname: Fang fullname: Fang, Zi-Yu organization: Department of Urology, Changhai Hospital, Second Military Medical University, Shanghai 200433, China – sequence: 19 givenname: Zhi-Peng surname: Xu fullname: Xu, Zhi-Peng organization: Department of Urology, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China – sequence: 20 givenname: Yi surname: Bao fullname: Bao, Yi organization: Department of Urology, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China – sequence: 21 givenname: Deng-Shuang surname: Wu fullname: Wu, Deng-Shuang organization: Department of Urology, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China – sequence: 22 givenname: Xiong surname: Miao fullname: Miao, Xiong organization: Department of Orthopedics, Changhai Hospital, Second Military Medical University, Shanghai 200433, China – sequence: 23 givenname: Hai-Yang surname: Sun fullname: Sun, Hai-Yang organization: Department of Orthopedics, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310009, China – sequence: 24 givenname: Ying-Hao surname: Sun fullname: Sun, Ying-Hao organization: Department of Urology, Changhai Hospital, Second Military Medical University, Shanghai 200433, China – sequence: 25 givenname: Hong-Yang surname: Wang fullname: Wang, Hong-Yang email: hywangk@vip.sina.com organization: The International Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Hospital, Second Military Medical University, Shanghai 200433, China – sequence: 26 givenname: Lin-Hui surname: Wang fullname: Wang, Lin-Hui email: wanglinhuicz@163.com organization: Department of Urology, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/27117758$$D View this record in MEDLINE/PubMed |
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| SubjectTerms | Animals Antineoplastic Agents - pharmacology Blotting, Northern Carcinoma, Renal Cell - blood Carcinoma, Renal Cell - drug therapy Carcinoma, Renal Cell - genetics Cell Line Cell Line, Tumor Disease-Free Survival Drug Resistance, Neoplasm - genetics Exosomes - genetics Gene Expression Profiling - methods Gene Expression Regulation, Neoplastic Humans Indoles - pharmacology Kidney Neoplasms - blood Kidney Neoplasms - drug therapy Kidney Neoplasms - genetics Mice, Nude MicroRNAs - genetics MicroRNAs - metabolism Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins c-met - genetics Pyrroles - pharmacology Receptor Protein-Tyrosine Kinases - genetics Reverse Transcriptase Polymerase Chain Reaction RNA, Long Noncoding - blood RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism RNA, Neoplasm - genetics RNA, Neoplasm - metabolism Signal Transduction - genetics Treatment Outcome Xenograft Model Antitumor Assays - methods |
| Title | Exosome-Transmitted lncARSR Promotes Sunitinib Resistance in Renal Cancer by Acting as a Competing Endogenous RNA |
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