MicroRNA-122 Inhibits Tumorigenic Properties of Hepatocellular Carcinoma Cells and Sensitizes These Cells to Sorafenib

MicroRNA122 is a key regulator of α-fetoprotein expression and influences the aggressiveness of hepatocellular carcinoma

“…The expression of miR122 and miR214 in mouse liver and human HCC tissues was examined by in situ hybridization 55,56 . Locked nucleic acid (LNA)-scramble (negative control) and LNA-anti-miR122 and LNA-anti-miR214 probes were obtained from EXIQON.…”

MiR-122 in hepatic function and liver diseases

“…Using a genome-wide expression profiling approach, Burchard et al (2010) have recently shown decreased miR-122 expression and increased miR-122 predicted target genes in tumor tissues compared with nontumor tissues from HCC, which may possibly lead to impairment of mitochondrial metabolism. Loss of miR-122 expression in HCC, which is associated with poor prognosis and metastasis, has been confirmed by several other studies (Coulouarn et al, 2009;Bai et al, 2009;Zeng et al, 2010;Mizuguchi et al, 2011;Karakatsanis et a., 2011). In these studies, miR-122 is shown to be involved in cell proliferation, apoptosis, clonogenic survival, migration, in vivo invasion, and tumor formation in nude mice.…”

HepatomiRNoma: The proposal of a new network of targets for diagnosis, prognosis and therapy in hepatocellular carcinoma

“…This action seems to be correlated with chronic viral infection. Besides in the study by Bai et al (2009) cell growth and survival of HCC cells expressing miR-122 were significantly reduced upon treatment with sorafenib, a multi-kinase inhibitor, which is actually approved for HCC patients. Li et al (2013), Fan et al (2011) showed that low miR-122 levels stimulated HBV replication and overexpression of viral antigen with subsequent cellular damage, overgrowth and hepatocellular fibrosis.…”

“…Other minor processes in which miR-122 is implicated seem to include the migration-related processes. Indeed low levels of miR-122 promote overexpression of disintegrin and metalloproteinase as ADAM17 (Tsai et al, 2009) and ADAM10 (Bai et al, 2009) that promote migration. This action seems to be correlated with chronic viral infection.…”