Neoplasma Vol.67, No.4, p.773–781, 2020
|
| Title: miR-3662 suppresses cell growth, invasion and glucose metabolism by targeting HK2 in hepatocellular carcinoma cells |
| Author: J. Ye, X. Xiao, Y. Han, D. Fan, Y. Zhu, L. Yang |
|
Abstract: Hepatocellular carcinoma (HCC) is one of the most common malignancies with a rising incidence around the world. MicroRNAs (miRNAs) have been reported to play essential roles in the progression of HCC. However, the precise mechanism of miR-3662 in the HCC process remains poorly understood. This study was aimed to determine the regulatory network of miR-3662 and hexokinase 2 (HK2) in HCC. Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to detect miR-3662 expression. Cell proliferation and invasion were measured by Cell Counting Kit-8 (CCK-8) assay and Transwell assay, respectively. Glucose consumption and lactate production assays were used to detect glucose metabolism activity in HCC cells. The potential binding sites between miR-3662 and HK2 were predicted by TargetScan online software and the relationship between miR-3662 and HK2 was verified by luciferase report assay. The protein expression of HK2 was measured by western blot analysis. A xenograft tumor model was established to confirm the role of miR-3662 and HK2 in vivo. miR-3662 expression was downregulated in HCC tissues and cells, and it was reduced in hypoxia-induced HCC cells in a time-dependent manner. Overexpression of miR-3662 or knockdown of HK2 inhibited cell proliferation, invasion, and glucose metabolism in HCC cells, which could be reversed by upregulating HK2. Besides, HK2 was a direct target of miR-3662 in HCC cells, and hypoxia upregulated the expression of HK2. In addition, the upregulation of HK2 could abolish miR-3662 overexpression-induced inhibitory effects on tumor growth and glucose metabolism in vivo.
|
|
| Keywords: hepatocellular carcinoma, hypoxia, miR-3662, HK2, growth, invasion, glucose metabolism |
|
|
Published online: 28-Jul-2020
|
| Year: 2020, Volume: 67, Issue: 4 |
Page From: 773, Page To: 781 |
doi:10.4149/neo_2020_190730N689
|
|
 download file |
|
|
|
|
