Role of microRNA-223 and its target gene oncogene c-myc in hepatocellular carcinoma pathogenesis.
10.3760/cma.j.issn.1007-3418.2011.02.010
- Author:
Wen-Yue ZHAO
1
;
Dong-Dong WANG
;
Meng-Qi SONG
;
Ling YANG
;
Jin YE
;
Li-Bo CHEN
Author Information
1. Digested Sections of Union Hospital of Huazhong University of Science and Technology, Wuhan 430022, China.
- Publication Type:Journal Article
- From:
Chinese Journal of Hepatology
2011;19(2):114-117
- CountryChina
- Language:Chinese
-
Abstract:
To investigate the regulatory role of microRNA-223 (miR-223) on c-myc and its role in hepatocarcinogenesis. miR-223 and c-myc mRNA expressions in normal tissue, paraneoplastic tissue, liver cancer tissue and liver cancer cells were tested with microRNA microarray and quantitative real-time PCR (qRT-PCR). C-myc protein expression was detected by Western blot. MiR-223 mimic was transfected into HepG2 cells and the expression changes of c-myc mRNA and protein were tested with qRT-PCR and Western blot respectively. MiR-223 was down-regulated by 61.53% and 30.77% respectively in hepatocellular carcinoma and adjacent tissues as compared to normal liver tissues and the expression of miR-223 was also decreased in HepG2 cell as compared to fetal liver cells L02, whereas the expressions of c-myc mRNA and protein increased in paraneoplastic and HCC tissues compared with normal liver tissues. It prompts that the expressions of miR-223 and c-myc are negatively correlated. No obvious difference found among c-myc mRNA expressions after miR-223 mimics transfection. The c-myc abnormal high-expression may play a dynamic role in hepatocarcinogenesis due to the miR-223 down-regulation.
