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miR-106b 通过靶向锌指和 BTB 结构域蛋白 7A(Zbtb7a)调节肝癌细胞的凋亡和肿瘤发生。

MiR-106b regulates the apoptosis and tumorigenesis of hepatocellular carcinoma via targeting Zinc finger and BTB domain-containing protein 7A (Zbtb7a).

机构信息

Department of Hepatobiliary Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, People's Republic of China.

Nursing Department, the First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, People's Republic of China.

出版信息

J Biochem Mol Toxicol. 2018 Aug;32(8):e22169. doi: 10.1002/jbt.22169. Epub 2018 Jul 5.

Abstract

MicroRNAs play vital regulatory roles in various type of tumorigenesis. We aimed to explore the functional microRNAs that might play as therapeutic targets in hepatocellular carcinoma (HCC). In this study, our results revealed that microRNA-106b was significantly increased in HCC tumor tissues. However, miR-106b knockdown remarkably suppressed the growth and increased the apoptosis of Hub-7 HCC cells. Biological analysis indicated that miR-106b directly targeted toZinc finger and BTB domain-containing protein 7A (Zbtb7a) to regulate the apoptosis of Hub-7 cells. Extensively, Zbtb7a overexpression reversed Huh-7 cell apoptosis and growth in vitro. Furthermore, in vivo studies confirmed that miR-106b inhibition or Zbtb7a overexpression retarded the growth of Hub-7 xenograft tumor in nude mice. In conclusion, we provide the evidence for the regulatory role of miR-106b in HCC, which is causally linked to targeting of Zbtb7a. This study may provide miR-106b as a potential therapeutic strategy for HCC.

摘要

MicroRNAs 在各种类型的肿瘤发生中发挥着重要的调节作用。我们旨在探索可能作为肝细胞癌 (HCC) 治疗靶点的功能性 microRNAs。在这项研究中,我们的结果表明 microRNA-106b 在 HCC 肿瘤组织中显著增加。然而,miR-106b 的敲低显著抑制了 Hub-7 HCC 细胞的生长并增加了其凋亡。生物学分析表明,miR-106b 可直接靶向 Zinc finger and BTB domain-containing protein 7A (Zbtb7a) 来调节 Hub-7 细胞的凋亡。此外,Zbtb7a 的过表达逆转了 Huh-7 细胞的体外凋亡和生长。此外,体内研究证实 miR-106b 的抑制或 Zbtb7a 的过表达可抑制裸鼠中 Hub-7 异种移植肿瘤的生长。总之,我们提供了 miR-106b 在 HCC 中起调节作用的证据,这与靶向 Zbtb7a 有关。这项研究可能为 HCC 提供 miR-106b 作为一种潜在的治疗策略。

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