AKT2型
肝细胞癌
癌基因
癌症研究
肝癌
肝细胞癌
医学
癌症
细胞生长
细胞
肿瘤科
生物
细胞周期
内科学
信号转导
AKT1型
PI3K/AKT/mTOR通路
遗传学
作者
Hongwei Li,Dawei Guo,Yuhong Zhang,Shiming Yang,Rui Zhang
出处
期刊:Cancer Biotherapy and Radiopharmaceuticals
[Mary Ann Liebert]
日期:2020-10-01
卷期号:35 (8): 605-614
被引量:10
标识
DOI:10.1089/cbr.2019.3043
摘要
Background: miR-664b-5p accelerates the development of certain cancers, but the role of miR-664b-5p in hepatocellular carcinoma (HCC) has been less reported. Therefore, the authors aimed to study the role of miR-664b-5p in HCC progression. Materials and Methods: miR-664b-5p expression in liver cancer and adjacent tissues, and in HepG2 and SUN-475 cells, was measured by quantitative real-time polymerase chain reaction (qRT-PCR). Relationship between miR-664b-5p and AKT2 was predicted by TargetScan and confirmed by dual-luciferase reporter assay, and gene or protein expressions were determined by performing qRT-PCR and Western blotting. The viability and apoptosis, and the migration and invasion of HepG2 and SUN-475 cells were determined by CCK-8 assay and flow cytometry, and transwell assay, respectively. Results: Downregulated miR-664b-5p was observed in hepatocellular cancer tissues. Functional analyses revealed that miR-664b-5p mimic suppressed viability, migration, and invasion, but promoted apoptosis in HepG2 and SUN-475 cells. AKT2 was a target of miR-664b-5p, whose mimics inhibited the expression of AKT2. However, upregulated AKT2 promoted viability, migration, and invasion, but inhibited apoptosis in HepG2 and SUN-475 cells, and such effects were reversed by miR-664b-5p mimics. Conclusions: miR-664b-5p acts as a cancer suppressor through negatively regulating AKT2 expression in HepG2 and SUN-475 cells, suggesting that miR-664b-5p could be a protective target for HCC patients.
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