Department of Hepatobiliary and Pancreatic Surgery, The Affiliated Huai'an No.1 People's Hospital of Nanjing Medical University, Huai'an, China.
Eur Rev Med Pharmacol Sci. 2019 Jan;23(2):567-575. doi: 10.26355/eurrev_201901_16869.
This study aimed at investigating whether miR-637 could promote proliferation of hepatocarcinoma cells by targeted regulation of AKT1 expression, leading to enhanced cell invasion and thus participating in the progression of liver cancer.
The miR-637 and AKT1 expressions in cancer tissues and adjacent tissues of liver cancer patients were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The effects of miR-637 on cell proliferation and cell invasion were examined by cell counting kit-8 (CCK-8) and cell invasion assays. Dual-luciferase reporter gene assay was performed to evaluate the regulating relationship between miR-637 and AKT1. Also, the expression of AKT1 after overexpression or knockdown of miR-637 was analyzed by Western blot to evaluate whether miR-637 could affect proliferative and invasive ability of hepatoma cells by inhibiting the expression of AKT1.
The qRT-PCR results revealed that miR-637 expression in cancer tissues of liver cancer patients was markedly lower than that in corresponding adjacent tissues, which was consistent with its low expression in HCC cell lines. However, AKT1 expression in cancer tissues was markedly higher than that in corresponding adjacent tissues. Overexpression of miR-637 in hepatoma cells inhibited cell proliferation and attenuated cell invasion, while inhibition of miR-637 showed the opposite effect. Results of dual-luciferase reporting assay and Western blot demonstrated that miR-637 can selectively degrade AKT1 and that overexpression of AKT1 in HCC cells can partially reverse the effect of miR-637 on cell proliferation and invasion.
MiR-637 can promote the proliferation of hepatoma cells and enhance invasive cell ability, the mechanism of which may be related to the targeted regulation of AKT1 expression.
本研究旨在探讨 miR-637 是否可以通过靶向调控 AKT1 表达促进肝癌细胞增殖，进而增强细胞侵袭能力，从而参与肝癌的进展。
采用实时定量聚合酶链反应（qRT-PCR）检测肝癌患者癌组织和癌旁组织中 miR-637 和 AKT1 的表达。通过细胞计数试剂盒-8（CCK-8）和细胞侵袭实验检测 miR-637 对细胞增殖和细胞侵袭的影响。双荧光素酶报告基因实验评估 miR-637 与 AKT1 之间的调控关系。Western blot 分析 miR-637 过表达或敲低后 AKT1 的表达，以评估 miR-637 是否可以通过抑制 AKT1 的表达来影响肝癌细胞的增殖和侵袭能力。
qRT-PCR 结果显示，肝癌患者癌组织中 miR-637 的表达明显低于相应癌旁组织，与 HCC 细胞系中低表达一致。然而，癌组织中 AKT1 的表达明显高于相应癌旁组织。肝癌细胞中 miR-637 的过表达抑制细胞增殖并减弱细胞侵袭，而 miR-637 的抑制则表现出相反的效果。双荧光素酶报告基因检测和 Western blot 结果表明，miR-637 可以选择性降解 AKT1，而 HCC 细胞中 AKT1 的过表达可以部分逆转 miR-637 对细胞增殖和侵袭的影响。
miR-637 可促进肝癌细胞的增殖并增强侵袭细胞能力，其机制可能与靶向调控 AKT1 表达有关。
