miR-210 的沉默通过靶向 EGR3 抑制肝癌和乙型肝炎病毒相关性肝癌的进展。
Silencing of microRNA-210 inhibits the progression of liver cancer and hepatitis B virus-associated liver cancer via targeting EGR3.
机构信息
The seventh Inpatient Area, Qingdao Sixth People's Hospital, No. 9, Fushun Road, Shibei District, Qingdao City, 266033, Shandong Province, China.
Department of Inspection, Qingdao Sixth People's Hospital, No. 9, Fushun Road, Shibei District, Qingdao City, 266033, Shandong Province, China.
出版信息
BMC Med Genet. 2020 Mar 6;21(1):48. doi: 10.1186/s12881-020-0974-9.
BACKGROUND
This study was aimed to investigate the regulatory role of microRNA-210 (miRNA-210) on the progression of liver cancer and Hepatitis B virus (HBV)-associated liver cancer.
METHODS
The expression of miRNA-210 was detected in liver tissues of HBV-associated cirrhosis and liver cancer, and in HepG2 and HepG2.2.15 cells by qRT-PCR. MiRNA-210 was silenced in HepG2 and HepG2.2.15 cells by the transfection of miRNA-210 inhibitor. The cell viability and apoptosis was detected by MTT assay and Annexin V-fluorescein isothiocyanate/propidium iodide staining, respectively. The protein expression of EGR3 was detected by Western blot. The regulatory relationship between EGR3 and miRNA-210 was predicted by TargetScan and identified by Dual luciferase reporter gene assay.
RESULTS
MiRNA-210 was overexpressed in the liver tissues of HBV-associated cirrhosis and liver cancer, and in HepG2 and HepG2.2.15 cells (P < 0.05). Silencing of miRNA-210 inhibited the viability and promoted the apoptosis of HepG2 and HepG2.2.15 cells (P < 0.05). EGR3 was a target of miRNA-210, which was down-regulated in the liver tissues of HBV-associated cirrhosis and liver cancer, and in HepG2 and HepG2.2.15 cells (P < 0.05). Silencing of miRNA-210 increased the mRNA and protein expression of EGR3 (P < 0.05). Silencing of EGR3 reversed the anti-tumor effect of miRNA-210 inhibitor on HepG2 and HepG2.2.15 cells (P < 0.05).
CONCLUSIONS
Silencing of miRNA-210 inhibits the progression of liver cancer and HBV-associated liver cancer via up-regulating EGR3.
背景
本研究旨在探讨 microRNA-210（miRNA-210）在肝癌和乙型肝炎病毒（HBV）相关肝癌进展中的调控作用。
方法
通过 qRT-PCR 检测 HBV 相关肝硬化和肝癌组织以及 HepG2 和 HepG2.2.15 细胞中 miRNA-210 的表达。通过 miRNA-210 抑制剂转染沉默 HepG2 和 HepG2.2.15 细胞中的 miRNA-210。通过 MTT 测定和 Annexin V-荧光素异硫氰酸酯/碘化丙啶染色分别检测细胞活力和细胞凋亡。通过 Western blot 检测 EGR3 的蛋白表达。通过 TargetScan 预测 EGR3 与 miRNA-210 的调控关系，并通过双荧光素酶报告基因检测进行鉴定。
结果
miRNA-210 在 HBV 相关肝硬化和肝癌组织以及 HepG2 和 HepG2.2.15 细胞中过度表达（P < 0.05）。沉默 miRNA-210 抑制 HepG2 和 HepG2.2.15 细胞的活力并促进其凋亡（P < 0.05）。EGR3 是 miRNA-210 的靶基因，在 HBV 相关肝硬化和肝癌组织以及 HepG2 和 HepG2.2.15 细胞中表达下调（P < 0.05）。沉默 miRNA-210 增加 EGR3 的 mRNA 和蛋白表达（P < 0.05）。沉默 EGR3 逆转了 miRNA-210 抑制剂对 HepG2 和 HepG2.2.15 细胞的抗肿瘤作用（P < 0.05）。
结论
沉默 miRNA-210 通过上调 EGR3 抑制肝癌和 HBV 相关肝癌的进展。
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