Recently, Scisciani and colleagues demonstrated that lipopolysaccharide, AZD1152-HQPA manufacturer lymphotoxin-α, and tumor necrosis factor-α inflammatory pathways activated miR-224 expression. In addition, these authors identified p65/NFκB as a direct transcriptional regulator of miR-224 expression.[36] In our study,

increased expression of miR-224 upon HCV reactivation is in accordance with the findings of Scisciani and colleagues,[36] as NFκB-dependent inflammatory pathway is a key process during HCV infection.[37] Increased expressions of miR-221, miR-224, and miR-217 were observed in samples taken after administration of IFN/RBV treatment as compared with the pretreatment samples. miR-224 was able to recognize OCLN as a target mRNA. miR-221 expression is dysregulated in HCC[38] and is suggested to be affected by HCV and IFN. Liu EGFR tumor and colleagues demonstrated that miR-221 was downregulated after HCV exposure, and the gain of miR-221 enhanced HCV RNA abundance in a dynamic in vitro HCV infection system.[9] Zhang and colleagues knocked down miR-221 and miR-222 in glioblastoma cells and reported that IFN-α was the most significantly affected signaling pathway.[39] Interestingly, we found that miR-221 expression level negatively correlated with HAI. miR-217 was previously shown to potentially predict therapy response in chronic HCV-infected patients[40] and was found to be related to tumor differentiation

as well.[14] We observed relevant alterations of microRNA expressions in the SVR group, whereas microRNA expression levels remained stable in non-responders after IFN/RBV treatment in comparison with pretreatment levels. Partial responders following completed antiviral therapy were only three patients; therefore, these patients were analyzed together within the NR group. It was recently revealed that hepatic microRNA expression could be associated with drug response[3]; however, our study did not reveal a predictive value of pretreatment microRNA levels, including miR-122, for the success of IFN/RBV treatment. Previously, Sarasin-Filipowicz and colleagues demonstrated markedly

decreased pretreatment miR-122 levels in patients who had no virological response during later IFN therapy.[31] Estrabaud and colleagues reported deregulated miR-99a*, miR-181a-2*, miR-23a, and selleck chemicals miR-217 in non-responders compared with patients with later SVR.[40] In contrast, our study revealed upregulated miR-96, miR-99a*, miR-122, miR-181a-2*, miR-217, and miR-221 expressions after IFN/RBV treatment in the SVR group when compared with the NR group. In addition, following antiviral treatment, miR-221 and miR-122 levels were higher in SVR when compared with pretreatment levels. This suggests that antiviral therapy restored miR-122 expression in SVR patients. miR-122 is considered a differentiation and homeostatis marker in hepatocytes.