| lncRNA PTPRG-AS1通过靶向miR-124-3p调控肝癌细胞凋亡和放射敏感性的研究机制 |
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| 引用本文： | 李敬霞1,刘 艳2. lncRNA PTPRG-AS1通过靶向miR-124-3p调控肝癌细胞凋亡和放射敏感性的研究机制[J]. 现代肿瘤医学, 2021, 0(10): 1676-1682. DOI: 10.3969/j.issn.1672-4992.2021.10.006 |
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| 作者姓名： | 李敬霞1 刘 艳2 |
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| 作者单位： | 1.河南科技大学第一附属医院肿瘤放疗科,河南 洛阳 471003；2.郑州大学第一附属医院核医学科,河南 郑州 450052 |
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| 摘 要： | 目的:探讨lncRNA PTPRG-AS1对肝癌细胞凋亡和放射敏感性的影响及作用机制。方法:培养正常肝细胞L02和肝癌细胞HepG2、SMMC-7721和BEL-7402，qRT-PCR检测细胞中PTPRG-AS1和miR-124-3p表达水平。转染si-PTPRG-AS1、miR-124-3p mimics至HepG2细胞，抑制HepG2细胞中PTPRG-AS1表达或过表达miR-124-3p，流式细胞术检测细胞凋亡，克隆形成实验检测细胞放射敏感性，Western Blot法检测Bcl-2和Bax蛋白表达。生物信息学软件预测PTPRG-AS1与miR-124-3p存在互补的核苷酸序列，双荧光素酶报告基因实验验证PTPRG-AS1与miR-124-3p之间的调控关系。结果:与正常肝细胞L02相比，肝癌细胞HepG2、SMMC-7721和BEL-7402中PTPRG-AS1表达显著升高（P＜0.05），miR-124-3p表达显著降低（P＜0.05）。抑制PTPRG-AS1或过表达miR-124-3p均可促进肝癌HepG2细胞的凋亡，增强肝癌HepG2细胞的放射敏感性，抑制Bcl-2蛋白表达，促进Bax蛋白表达。PTPRG-AS1负调控miR-124-3p表达。抑制miR-124-3p表达可部分逆转抑制PTPRG-AS1表达对肝癌HepG2细胞凋亡的促进作用以及放射敏感性的增强作用。结论:抑制PTPRG-AS1表达可能通过上调miR-124-3p表达促进肝癌细胞的凋亡并提高其放射敏感性，是肝癌治疗的潜在作用靶点。
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| 关 键 词： | 肝癌 lncRNA PTPRG-AS1 miR-124-3p 细胞凋亡 放射敏感性 |
LncRNA PTPRG-AS1 regulates apoptosis and radiosensitivity of hepatoma cells by targeting miR-124-3p |
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| LI Jingxia1,LIU Yan2. LncRNA PTPRG-AS1 regulates apoptosis and radiosensitivity of hepatoma cells by targeting miR-124-3p[J]. Journal of Modern Oncology, 2021, 0(10): 1676-1682. DOI: 10.3969/j.issn.1672-4992.2021.10.006 |
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| Authors: | LI Jingxia1 LIU Yan2 |
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| Affiliation: | 1.Department of Oncology Radiotherapy,the First Affiliated Hospital of Henan University of Science and Technology，Henan Luoyang 471003,China;2.Department of Nuclear Medicine,the First Affiliated Hospital of Zhengzhou University，Henan Zhengzhou 450052,China. |
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| Abstract: | Objective:To investigate the effect of lncRNA PTPRG-AS1 on apoptosis and radiosensitivity of hepatoma cells and its mechanism.Methods:Normal liver cells L02 and hepatoma cells HepG2,SMMC-7721 and BEL-7402 were cultured,and the expression level of PTPRG-AS1 and miR-124-3p were detected by qRT-PCR.si-PTPRG-AS1 or miR-124-3p mimics were transfected into HepG2 cells in order to obtain HepG2 cells with inhibition of PTPRG-AS1 expression or overexpression of miR-124-3p.Then papoptosis was detected by flow cytometry.Cellular radiosensitivity was detected by colony formation assay,and Bcl-2 and Bax protein expression was detected by Western Blot.The bioinformatics software predicted the existence of a complementary nucleotide sequence between PTPRG-AS1 and miR-124-3p,and the dual luciferase reporter gene assay verified the regulatory relationship between PTPRG-AS1 and miR-124-3p.Results:Compared with normal liver cell L02,the expression level of PTPRG-AS1 in HepG2,SMMC-7721 and BEL-7402 was significantly increased (P＜0.05),and the expression level of miR-124-3p was significantly decreased (P＜0.05).Inhibition of PTPRG-AS1 or overexpression of miR-124-3p promoted apoptosis of HepG2 cells,enhanced the radiosensitivity of HepG2 cells,inhibited Bcl-2 protein expression and promoteed Bax protein expression.PTPRG-AS1 negatively regulated miR-124-3p expression.Inhibition of miR-124-3p expression partially reversed the effects of inhibition of PTPRG-AS1 expression on the apoptosis promotion and the enhancement of radiosensitivity of hepatocellular carcinoma HepG2 cells.Conclusion:Inhibition of PTPRG-AS1 expression may promote the apoptosis of hepatoma cells and increase its radiosensitivity by up-regulating the expression of miR-124-3p,which is a potential target for the treatment of liver cancer. |
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| Keywords: | liver cancer lncRNA PTPRG-AS1 miR-124-3p apoptosis radiosensitivity |
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