The role of microRNA-155 in the development and diagnosis of liver disease

microRNA(miRNA)is a type of single-stranded small molecule non-coding RNA that interacts with the 3'untranslated region of the target gene to achieve negative regulation of the target gene and participate in multiple links of cell proliferation and apoptosis.At present,there is evidence that miRNA-155 is involved in the occurrence and development of a variety of liver diseases.By consulting relevant literature reports,this article summarizes the effects of miRNA-155 in non-alcoholic fatty liver disease,alcoholic liver disease,viral hepatitis,acute liver failure,and liver disease.The research progress of fibrosis and liver cancer in a variety of liver diseases,and the potential of miRNA-155 as a non-invasive biomarker is analyzed to provide a reference for exploring the diagnosis and treatment of liver diseases.

Vitamin C exerts anti-cadmium induced fracture functions/targets:bioinformatic and biostructural findings

Background:Epidemiological data indicate an association between cadmium exposure and risk of bone fracture;however,clinical treatment of cadmium-induced fracture is limited.Although vitamin C(VC)reportedly reduces cadmium-induced fracture,its pharmacological mechanism remains unexplored.Methods:Thus,we used a network pharmacology approach and molecular docking analysis to identify core targets,functional processes,and biological pathways involved in the anti-fracture action of VC.Results:Bioinformatics identified 17 intersection targets of VC and cadmium-induced fracture,Nine core targets were characterized,including tumor protein p53,epidermal growth factor receptor,proto-oncogene c,mitogen-activated protein kinase-1(MAPK1),MAPK3,signal transducer and activator of transcription-3,MAPK14,prostaglandin-endoperoxide synthase 2,and estrogen receptor alpha.Interestingly,findings of molecular docking analysis indicated that VC exerted effective binding capacity in cadmium-induced fracture.Furthermore,biological processes,cell components,molecular functions,and pharmacological pathways involved in the action of VC against cadmium-induced fracture were identified and visualized.Conclusions:Based on these findings,we conclude that VC exhibits its anti-cadmium-induced fracture effects by promoting osteoblastic regeneration and proliferation,and inhibiting inflammatory stress.The core targets may serve as biomarkers for diagnosing cadmium-induced fractures.

Anti-hepatic carcinoma mechanisms of calycosin through targeting ferroptosis

Background Ferroptosis,a pathologic state induced by lipid-driven oxidative stress,is associated with the development of human cancers.Calycosin,a natural compound with antioxidant and anti-inflammatory activities,has promising antitumor effects.However,the ferroptosis-related mechanism of calycosin in the treatment of hepatic carcinoma has not been reported.Methods This study applied network pharmacology and bioinformatic approaches(including Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis)to investigate the pharmacologic targets and mechanism of action of calycosin in the treatment of hepatic carcinoma through targeting ferroptosis.By searching online databases including The Cancer Genome Atlas,FerrDb,GeneCards,SwissTargetPrediction,SuperPred,BindingDB,TargetNet,BATMAN-TCM,and Drugbank,we identified 13 ferroptosis-related putative target genes of calycosin against hepatic carcinoma including IL-6,PTGS2,SRC,HRAS,NQO1,NOX4,PGK1,G6PD,GPI,MIF,NOS2,ALDOA,and SQSTM1.Results Molecular docking analysis revealed that calycosin potentially binded directly with the target proteins IL-6,PTGS2,and SRC.Functional enrichment analysis of these proteins indicated that they were involved in gluconeogenesis and apoptosis through regulation of ERK1,ERK2,and MAPK activities(P<0.05).Conclusion Calycosin exerts antitumor effects in hepatic carcinoma by targeting ferroptosis through regulation of IL-6,PTGS2,and SRC.