Current Condition Regarding LNA Inhibitor in microRNA miR-23b Cell Proliferation and Apoptosis Induces as a Potential Therapeutic Option in Treatment of Human Hepatocellular Carcinoma

Dysregulation of microRNAs (miRNAs) has been shown to be involved in the pathogenesis and advances of many malignancies. Human hepatocellular carcinoma (HCC) is one of the most common cancers worldwide and the third cause of cancer related deaths. Recent data suggest that microRNA-23b (miR-23b) is significantly elevated in different types of cancer, particularly human hepatocellular carcinoma. locked nucleic acid (LNA) modified oligonucleotides have recently been suggested as a novel approach for targeting miRNAs as antisense based gene silencing. The aim of this study was to explore the functional role of LNA-antimiR-23b in a HepG2 (hepatocarcinoma) cell line. HepG2 cells were transfected with LNA-anti-miR-23b for 24, 48 and 72h. Quantitative real-time reverse transcriptase-PCR (qRT-PCR) was performed to assess miR-23b expression by LNA-anti-miR-23b. The viability of the cells was evaluated by MTT (3-[4, 5-dimethylthiazol-2-yl]-2, 5-diphenyl tetrazolium bromide) assay was used to realize apoptosis. LNA-anti-miR-23b was successfully transfected in human HepG2 cells and suppressed the miR-23b. LNA-anti-miR-23b inhibited the cells growth followed by induction of apoptosis. LNA-anti-miR-23b reduced the invasive behaviors of HepG2 cells after 24 h, compared with untreated cells and scrambled LNA-transfected cells and this effect was more pronounced after 72 h. Our findings suggest that inhibition of miR-23b could be used as a novel approach in treatment of HCC.

Keywords:

microRNA , miR-23b , human hepatocellular carcinoma , Locked Nucleic Acid