Small nucleolar RNAs (SnoRNAs) are a class of non-coding RNAs divided into two classes: C/D box snoRNAs and H/ACA box snoRNAs. The canonical function of C/D box and H/ACA box snoRNAs are 2'- O -ribose methylation and pseudouridylation of ribosomal RNAs (rRNAs), respectively. Emerging evidence has demonstrated that snoRNAs are involved in various physiological and pathological cellular processes. Mutations and aberrant expression of snoRNAs have been reported in cell transformation, tumorigenesis, and metastasis, indicating that snoRNAs may serve as biomarkers and/or therapeutic targets of cancer. Hence, further study of the functions and underlying mechanism of snoRNAs is valuable. In this review, we summarize the biogenesis and functions of snoRNAs, as well as the association of snoRNAs in different types of cancers and their potential roles in cancer diagnosis and therapy.

Background and Aims The evolution and clinical significance of abnormal liver chemistries and the impact of hepatitis B infection on outcome in patients with COVID-19 is not well characterized. This study aimed to explore these issues. Methods This large retrospective cohort study included 2073 patients with COVID-19 having definite outcomes in Wuhan, China. Longitudinal liver function tests were conducted and determined their associated factors and death risk by multivariate regression analyses. A prognostic nomogram was formulated to predict the survival of patients with COVID-19. The characteristics of liver abnormalities and outcomes of patients with COVID-19 with and without hepatitis B were compared after 1:3 propensity score matching. Results Of the 2073 patients, 1282 (61.8%) had abnormal liver chemistries during hospitalization, and 297 (14.3%) had a liver injury. The mean levels of AST and D-Bil increased early after symptom onset in deceased patients and showed disparity compared with that in discharged patients throughout the clinical course of the disease. Abnormal admission AST (adjusted hazard ratio [HR]: 1.39, 95%CI: 1.04-1.86, P =0.027) and D-Bil (adjusted HR: 1.66, 95%CI: 1.22-2.26, P =0.001) levels were independent risk factors for mortality due to COVID-19. A nomogram was established based on the results of multivariate analysis and showed sufficient discriminatory power and good consistency between the prediction and the observation. HBV infection in patients did not increase the risk of COVID-19-associated poor outcomes. Conclusions Abnormal AST and D-Bil levels at admission were independent predictors of COVID-19 mortality. Therefore, monitoring liver chemistries, especially AST and D-Bil levels, in hospitalized patients with COVID-19, is necessary.

Doxorubicin (Dox), an antitumor antibiotic, has therapeutic effects on many kinds of tumors. However, Dox can produce some serious side effects that limit its clinical application. Thus, exploration of effective drug targets or active lead compounds against Dox-induced organ damage is necessary. Dioscin, one natural product, has potent effects against Dox-induced renal injury and cardiotoxicity. However, the effects of dioscin on Dox-induced hepatotoxicity have not been reported. In this study, the results showed that dioscin significantly ameliorated Dox-induced cell injury, reduced reactive oxygen species (ROS) level, and suppressed cell apoptosis in alpha mouse liver 12 (AML-12) cells caused by Dox. In vivo, dioscin evidently decreased the levels of alanine transaminase (ALT), aspartate transaminase (AST), malondialdehyde (MDA); increased the levels of superoxide dismutase (SOD), glutathione (GSH), and glutathione peroxidase (GSH-Px); and alleviated liver injury. Mechanism study showed that dioscin remarkably up-regulated the expression levels of silent information regulator 1 (Sirt1) and heme oxygenase-1 (HO-1) via increase of the nuclear translocation of NF-E2-related factor 2 (Nrf2) and suppressed the expression levels of forkhead box protein O1 (FOXO1) and kelch-like ECH-associated protein-1 (Keap1) to inhibit oxidative stress. Furthermore, dioscin obviously decreased the nuclear translocation of nuclear factor κB (NF-κB) and the mRNA levels of tumor necrosis factor alpha (TNF-α), interleukin 1β (IL-1β), and interleukin 6 (IL-6) to suppress inflammation. Meanwhile, dioscin significantly regulated tumor suppressor P53 (P53) expression level and BCL-2-associated X (BAX)/BCL-2 apoptosis regulator (BCL-2) ratio to inhibit cell apoptosis. These results were further validated by knockdown of Sirt1 using siRNA silencing in AML-12 cells, which confirmed that the target of dioscin against Dox-induced hepatotoxicity was Sirt1/FOXO1/NF-κB signal. In short, our findings showed that dioscin exhibited protective effects against Dox-induced liver damage via suppression of oxidative stress, inflammation, and apoptosis, which should be developed as one new candidate for the prevention of Dox-induced liver injury in the future.