Upregulated expression of miR-106a by DNA hypomethylation plays an oncogenic role in hepatocellular carcinoma
- 379 Downloads
Aberrant microRNA (miRNA) expression has been widely recognized to play an extremely important role in several cancers, including hepatocellular carcinoma (HCC). According to the previous studies, abnormal miR-106a expression was closely related to various cancer occurrences. However, the miR-106a expression in HCC remains unclear. In our study, we firstly detected the miR-106a expression levels in 36 pairs of HCC tissues. The results showed that miR-106a expression in HCC tissues was apparently higher than the level in the adjacent tissues. Then, we used quantitative real-time PCR (qPCR) and BSP to analyze miR-106a expression and promoter methylation in HCC cell lines. There came to a conclusion that the methylation status of the miR-106a promoter region was inversely correlated with the expression of miR-106a. After prediction with online software, we further used dual-luciferase reporter gene assay to ensure that TP53INP1 and CDKN1A might be the direct targets of miR-106a. At last, we explored the functions of miR-106a in HCC cells in vitro. Our results manifested that high-miR-106a cell line had stronger invasiveness, faster cell cycle progression, and more resistance to apoptosis compared with the low-miR-106a cell line. Therefore, our study suggested that upregulated expression of miR-106a by its promoter hypomethylation might contribute to the progression of HCC, which might be considered as a potentially effective biomarker and therapeutic approach in the future.
KeywordsmiR-106a Hypomethylation Oncogene Hepatocellular carcinoma
This study was supported by a grant from the National Youthful Science Foundation of China (Nos. 81302145 and 81302147) and the National Science Foundation of Jiangsu Province, China (Nos. BK20130268 and 20130270).
Conflicts of interest
- 15.Jackson RJ, Standart N. How do microRNAs regulate gene expression? Sci STKE. 2007;2007(367):re1. doi: 10.1126/stke.3672007re1.