Inhibition of the invasion and migration of hepatocellular carcinoma cells by miR-148a and the mechanisms
10.3969/j.issn.1007-3969.2014.06.003
- VernacularTitle:miR-148a对肝癌细胞株侵袭和迁移的抑制作用及机制
- Author:
Xiaoqin JIA
;
Junjun MIAO
;
Jun YONG
;
Zilan ZHANG
;
Chen HUA
;
Guoli LI
- Publication Type:Journal Article
- Keywords:
miR-148a;
Hepatocellular carcinoma cell;
Invasion;
Migration;
MMP-2;
MMP-9
- From:
China Oncology
2014;(6):412-417
- CountryChina
- Language:Chinese
-
Abstract:
Background and purpose: Primary liver cancer is the malignant tumor of liver cells or intrahepatic bile duct epithelium with familiar metastasis and postsurgical recurrence. The purpose of this study was to investigate the effects of miR-148a on the invasion and migration of hepatocellular carcinoma cells and the underlying mechanisms. Methods: The supernatant containing LV-miR-148a lentivirus particles was used to infect SMMC-7721 cells. The expression of miR-148a was determined by RT-PCR. Wound healing assay and transwell assay were performed to detect the effects of miR-148a on the invasion of hepatocellular carcinoma cells. Gelatin zymography assay was used to detect the effects of miR-148a on the enzyme activities of matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9). The expression of MMP-2, MMP-9, E-cadherin and vimentin proteins was detected by Western blot assay. Results:RT-PCR showed the expression of miR-148a was upregulated in the infected SMMC-7721 cells. Transwell assay and wound healing assay showed ectopic expression of miR-148a suppressed cell migration and invasion abilities. miR-148a overexpression led to the decrease of the enzyme activities of MMP-2 and MMP-9 (P<0.05). Western blot assay showed that the protein expression of MMP-2, MMP-9 and vimentin proteins was signiifcantly decreased, the expression of E-cadherin had no changes. Conclusion:miR-148a is able to inhibit the migration and invasion of human SMMC-7721 cells in vitro, and the possible mechanisms may be related to decrease the enzyme activities of the MMP-2 and MMP-9 and the down regulation expression of MMP-2, MMP-9 and vimentin.
