miR-223-3p predicts prognosis of hepatitis B virus-related acute-on-chronic liver failure and is involved in hepatocyte injury via HSP90B1

Hepatitis B virus-related acute-on-chronic liver failure (HBV-ACLF) is a clinical syndrome that presents with acute hepatic decompensation and liver failure in a relatively short time, with a high mortality rate. The aim was to assess the predictive value of miR-223-3p in the short-term prognosis of patients and its potential role in HBV-ACLF, thus providing new ideas for personalized treatment. The level of miR-223-3p was quantified using qRT-PCR. The correlation between miR-223-3p level and indicators associated with the severity of HBV-ACLF (TBil, INR, and MELD score) was assessed using Spearman’s method. The prognostic value of miR-223-3p in HBV-ACLF was assessed using the ROC curve, Cox regression analysis, and Kaplan-Meier curve. To detect the proliferation and apoptosis of MIHA cells, CCK-8 assay and flow cytometry were employed. Bioinformatics methods were conducted to identify the downstream targets of miR-223-3p. The regulation between miR-223-3p and HSP90B1 was validated through Dual-luciferase reporter gene assay. In patients with HBV-ACLF, miR-223-3p expression was reduced and negatively correlated with TBil, INR, and MELD score. Low expression of miR-223-3p predicted adverse prognosis for patients. Furthermore, MELD score and miR-223-3p were identified as independent prognostic factors in patients with HBV-ACLF. In H2O2 or TNF-α–induced MIHA cells, miR-223-3p facilitated cellular proliferation and suppressed apoptosis. The role of miR-223-3p in hepatocyte injury was mediated by HSP90B1. Serum miR-223-3p expression was predictive for short-term survival in patients with HBV-ACLF, and miR-223-3p attenuated hepatocellular injury in vitro by modulating HSP90B1.