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长链非编码RNA TUG1通过吸附miR-145对XB1702细胞放射敏感性影响
引用本文:刘秀玲,王森,王志红,李静,陈新宇,贺全勤. 长链非编码RNA TUG1通过吸附miR-145对XB1702细胞放射敏感性影响[J]. 中华放射肿瘤学杂志, 2019, 28(12): 939-941. DOI: 10.3760/cma.j.issn.1004-4221.2019.12.013
作者姓名:刘秀玲  王森  王志红  李静  陈新宇  贺全勤
作者单位:驻马店市中心医院妇科 463000; 驻马店市中心医院放疗科 463000; 郑州大学第二附属医院妇产科 450000; 郑州大学第三附属医院妇产科 450000; 驻马店市中心医院肿瘤科 463000
摘    要:目的 研究长链非编码RNA TUG1对宫颈癌细胞放射敏感性的影响,并探讨其作用机制。方法 运用qRT-PCR法检测宫颈癌细胞XB1702及正常子宫内膜基质细胞ESC中TUG1和miR-145表达。实验分为转染si-NC组、转染si-TUG1、转染si-NC并照射、转染si-TUG1并照射、共转染si-TUG1和anti-miR-NC和共转染si-TUG1和anti-miR-145组。用脂质体法转染至XB1702细胞。克隆形成实验检测各组细胞存活分数,流式细胞术检测各组细胞凋亡。双荧光素酶报告基因检测各组细胞荧光活性。结果 与ESC细胞相比,XB1702细胞中TUG1表达升高,miR-145表达降低;沉默TUG1可显著提高XB1702细胞存活分数、促进凋亡,增强放射敏感性。TUG1可靶向调控miR-145表达,抑制miR-145可逆转沉默TUG1对XB1702细胞的增殖抑制、凋亡促进及增敏作用。结论 沉默长链非编码RNA TUG1可增强宫颈癌细胞放射敏感性,其机制可能与靶向miR-145有关,将可为宫颈癌放疗提供靶点。

关 键 词:TUG1基因   miR-145基因   放射敏感性   宫颈癌细胞系  
收稿时间:2019-02-23

Effect of long-chain non-coding RNA TUG1 on radiosensitivity of human cervical cancer XB1702 cells by adsorption of miR-145
Liu Xiuling,Wang Sen,Wang Zhihong,Li Jing,Chen Xinyu,He Quanqin. Effect of long-chain non-coding RNA TUG1 on radiosensitivity of human cervical cancer XB1702 cells by adsorption of miR-145[J]. Chinese Journal of Radiation Oncology, 2019, 28(12): 939-941. DOI: 10.3760/cma.j.issn.1004-4221.2019.12.013
Authors:Liu Xiuling  Wang Sen  Wang Zhihong  Li Jing  Chen Xinyu  He Quanqin
Affiliation:Department of Gynaecology,Zhumadian Central Hospital,Zhumadian 463000,China; Department of Radiotherapy,Zhumadian Central Hospital,Zhumadian 463000,China; Department of Obstetrics and Gynecology,Second Affiliated Hospital of Zhengzhou University,450000 Zhengzhou,China; Department of Obstetrics and Gynecology,Third Affiliated Hospital of Zhengzhou University,Zhengzhou 450000,China; Department of Oncology,Zhumadian Center Hospital,Zhumadian 463000,China
Abstract:Objective To evaluate the effect of long-chain non-coding RNA TUG1 on the radiosensitivity of cervical cancer cells and explore its underlying mechanism. Methods The expression of TUG1 and miR-145 in cervical cancer cells XB1702 and normal endometrial stromal cells (ESCs) was detected by qRT-PCR. The transfected si-NC,transfected si-TUG1,transfected si-NC combined with irradiation,transfected si-TUG1 combined with irradiation,si-TUG1 and anti-miR-NC co-transfected and,si-TUG1 and anti-miR-145 co-transfected groups were established, which were transfected into XB1702 cells by liposome method. The survival fraction of each group was detected by colony formation assay. The cell apoptosis of each group was detected by flow cytometry. The fluorescence activity of each group was assessed by dual luciferase reporter gene assay. Results Compared with the normal ESCs,the expression of TUG1 was significantly up-regulated, whereas that of miR-145 was significantly down-regulated in the cervical cancer cells XB1702. Silencing TUG1 significantly increased the survival fraction of XB1702 cells,promoted cell apoptosis and enhanced the radiosensitivity of irradiation to XB1702 cells. TUG1 could target and regulate the expression of miR-145. Suppressing miR-145 reversed the silencing effect of TUG1 on inhibiting proliferation, accelerating apoptosis promotion and enhancing sensitization of XB1702 cells. Conclusions Silencing long-chain non-coding RNA TUG1 can enhance the radiosensitivity of cervical cancer cells. The mechanism may be related to targeting miR-145,which will provide a target for radiotherapy of cervical cancer.
Keywords:TUG1 gene   miR-145 gene   Radiosensitivity   Cervical cancer cell line  
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