Hepatocellular carcinoma (HCC) is one of the most common and dangerous malignant tumors in China, which causes a large number of deaths every year. MicroRNAs (miRNAs) dysfunction contributes to the malignant progression of tumors. The aim of our study was to investigate the relationship between the biological role of miR-425-5p and malignant progression of HCC. Our results showed that miR-425-5p expression was significantly upregulated in HCC tissues and closely related to the poor prognosis of HCC patients. The knockdown of miR-425-5p inhibited cell proliferation and migration. Further, we identified RNF11 as the downstream target gene of miR-425-5p. In addition, the rescue experiments showed that the upregulation of RNF11 could rescue the inhibitory effect of miR-425-5p on HCC. In general, miR-425-5p as an oncogene promotes the malignant development of HCC via RNF11 and serves as a molecular target for predicting the prognosis of HCC patients.

Aim: To explore the hepatoprotective effects and mechanism of miRNA-544 in septic mice, C57BL/6J mice were intraperitoneally injected with lipopolysaccharide (LPS, 5 mg/kg) and treated with miR-544 inhibitors and mimics. Methods: The aspartate aminotransferase (AST), alanine aminotransferase (ALT) activities and total bilirubin (TBIL) levels were measured by automatic biochemical analyzer. The expression of proteins (MCP-1, CD16/32 and NF-κB inflammatory signaling pathways) and genes (inflammatory factors TNF-α, IL-6 and IL-1β)were measured by immunohistochemistry, western blot, qRT-PCR and ELISA. Results:The results indicated that miR-544 significantly reduced the level of ALT, AST and TBIL in serum and liver. Meanwhile, miR-544 attenuated the aggravation of inflammation by inhibiting MCP-1 and CD16/32, and suppressed IKK/NF-κB signal pathway by inhibiting the phosphorylation of IKK, IκB and NF-κB, thereby affecting the expression of inflammatory factors. Conclusions: miR-544 can attenuate LPS-induced liver injury in mice with sepsis via inhibiting the IKK/NF-κB signal pathway, and it is a potential candidate marker and therapeutic target for sepsis-induced liver injury.