Jingyu Zhang1, Qingbo Lu2, Haigang Pang3, Min Zhang4, Wenhai Wei5. 1. Department of Urology, The Fourth People's Hospital of Shenyang Shenyang 110031, Liaoning Province, China. 2. Department of Emergency, Ningyang County First People's Hospital Tai'an 271400, Shandong Province, China. 3. Department of Urology, The 971st Hospital of Chinese People's Liberation Army Navy Qingdao 266071, Shandong Province, China. 4. Department of Geriatrics, Sishui County People's Hospital Ji'ning 273200, Shandong Province, China. 5. Department of Anesthesiology, Shouguang Maternal and Child Care Hospital Weifang 262700, Shandong Province, China.
Abstract
OBJECTIVE: We investigated the mechanism of miR-103a-3p-mediated renal cell carcinoma (RCC) progression. METHODS: The miR-103a-3p expressions were measured in clinical samples and in two RCC cell lines. MiR-103a-3p was inhibited or over-expressed in the 786-O and UO31 cell lines, respectively. RESULTS: We found that miR-103a-3p is closely related to the development of RCC cells. A bioinformatics analysis and a dual-luciferase reporter gene assay revealed that there is a direct interaction between TMEM33 and miR-103a-3p. Moreover, a rescue assay further confirmed that TMEM33 overexpression can attenuate miR-103a-3p-induced RCC cell development. CONCLUSION: miR-103a-3p exerts a carcinogenic function in RCC by regulating TMEM33, a finding that may provide new insights into the development of prognostic markers and therapeutic targets for RCC. AJTR
OBJECTIVE: We investigated the mechanism of miR-103a-3p-mediated renal cell carcinoma (RCC) progression. METHODS: The miR-103a-3p expressions were measured in clinical samples and in two RCC cell lines. MiR-103a-3p was inhibited or over-expressed in the 786-O and UO31 cell lines, respectively. RESULTS: We found that miR-103a-3p is closely related to the development of RCC cells. A bioinformatics analysis and a dual-luciferase reporter gene assay revealed that there is a direct interaction between TMEM33 and miR-103a-3p. Moreover, a rescue assay further confirmed that TMEM33 overexpression can attenuate miR-103a-3p-induced RCC cell development. CONCLUSION: miR-103a-3p exerts a carcinogenic function in RCC by regulating TMEM33, a finding that may provide new insights into the development of prognostic markers and therapeutic targets for RCC. AJTR
Authors: B Escudier; C Porta; M Schmidinger; N Rioux-Leclercq; A Bex; V Khoo; V Grünwald; S Gillessen; A Horwich Journal: Ann Oncol Date: 2019-05-01 Impact factor: 32.976
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