To the best of our knowledge, the present study is the first to suggest the important roles of the H19/let‑7/Lin28 ceRNA network in BC autophagy and EMT, thus providing insight for the use of these molecules as prognostic biomarkers and therapeutic targets in BC metastasis.Gout is a common type of inflammatory arthritis that is clinically and genetically heterogeneous. The genetic aetiology remains unclear, and mainly relies on previous genome‑wide association studies focused on sporadic cases. The present study aimed to identify the genetic basis of gout in three families using whole‑exome sequencing (WES). WES was performed in the probands, and family members were involved in the co‑segregation analysis. In total, three deleterious rare or novel missense mutations were identified in ATP‑binding cassette super‑family G member 2 (ABCG2), protein kinase CGMP‑dependent 2 (PRKG2) and adrenoceptor β3 (ADRB3) genes in three different families. In addition, certain gout‑associated candidate genes were revealed to be shared among the co‑expression and protein‑protein interaction (PPI) networks of ABCG2, PRKG2 and ADRB3.  https://www.selleckchem.com/products/protac-tubulin-degrader-1.html  Furthermore, the disease ontology analysis of the genes present in the co‑expression network exhibited significant (P less then 0.05) enrichment in hyperuricemia, gout, cardiovascular system disease and metabolic disease. In addition, genes involved in the PPI network were significantly enriched in the purine nucleoside monophosphate biosynthetic process, urate transport and biological processes associated with glycose metabolism. Collectively, to the best of our knowledge, the present study was the first to use WES to identify three candidate rare or novel deleterious mutations in three families with gout. The present results provided novel insights that may improve the current understanding of the molecular genetic basis underlying gout. Importantly, the present results may facilitate the improvement of clinical diagnosis and the development of novel personalized therapies.Tumor necrosis factor‑associated apoptosis‑inducing ligand (TRAIL) is considered to be a potential therapeutic target for various types of cancer. However, colon cancer is difficult to treat due to its resistance to TRAIL. Therefore, various trials have been conducted to overcome TRAIL resistance in colon cancer. The present study aimed to determine whether icariin (ICA) may sensitize human colon cancer cells to TRAIL‑induced apoptosis in vitro and in vivo. In the investigation of the effect of ICA on TRAIL‑induced apoptosis, the LIVE/DEAD assay results demonstrated that TRAIL plus ICA synergistically induced apoptosis in 49% of HCT116 colon cancer cells. These results were confirmed using long‑term colony formation assay. ICA potentiated TRAIL‑induced apoptosis by modulating the expression of apoptotic proteins and the induction of cell surface death receptors (DRs) 4 and 5. Upregulation of DRs by ICA was also observed at the transcriptional level by RT‑PCR. The expression of DR by ICA was increased through the production of reactive oxygen species (ROS). The results also suggested that increased expression of DR by ICA may be due to the activation of ERK and induction of the transcription factor CCAAT enhancer‑binding protein homologous protein (CHOP). NAC, a ROS scavenger, reduced the effect of ICA on ERK activation, DR induction and sensitization of TRAIL‑induced apoptosis. In addition, ICA enhanced the effects of TRAIL to reduce tumor growth in an in vivo xenograft mouse model. Overall, the present study provided evidence that ICA sensitized tumor cells to TRAIL‑induced apoptosis via ROS‑, ERK‑ and CHOP‑mediated upregulation of DR5 and DR4. Based on these results, it is suggested that the antitumor activity of ICA and TRAIL co‑treatment in vitro and in vivo may be used as an effective therapeutic agent in chemotherapy.Carbon monoxide‑releasing molecule‑3 (CORM‑3), which is an exogenous carbon monoxide (CO) compound, slowly releases CO under physiological conditions; this exerts neuroprotective effects against incomplete ischemia/reperfusion injury. The objective of the present study was to investigate whether the administration of CORM‑3 protects against nucleotide‑binding oligomerization domain‑like receptor pyrin domain‑3 (NLRP3) inflammasome formation and neuronal pyroptosis in the hippocampus following hemorrhagic shock and resuscitation (HSR). To establish this, an HSR model was created. Hemorrhagic shock was induced in adult male Sprague‑Dawley rats under sevoflurane anesthesia by bleeding using a heparinized syringe to maintain a mean arterial pressure of 30±5 mmHg for 60 min. Resuscitation was performed by reperfusion of the blood and, if necessary, administering sterile saline to achieve the baseline arterial pressure. Following resuscitation, CORM‑3 (4 mg/kg) was injected via the femoral vein. Neuronal pyroptosis in the hippocampus, mitochondrial morphology, mitochondrial DNA (mtDNA), brain magnetic resonance imaging, expression levels of NLRP3 and the interaction of pro‑caspase‑1 and apoptosis‑associated speck‑like protein containing a CARD domain (ASC) were examined 12 h after HSR; locomotor activity was assessed 7 days after HSR. Compared with HSR‑treated rats, CORM‑3 administration resulted in a lower level of neuronal pyroptosis in the hippocampus, improved mitochondrial morphology, a lower mtDNA level, steadier levels of metabolites, decreased expression levels of NLRP3 and pro‑caspase‑1 interacting with ASC and enhanced locomotor activity. In conclusion, treatment with CORM‑3 ameliorated impairments of locomotor and exploratory activities in a rat model of HSR. The mechanism may be associated with the inhibition of mitochondrial DNA‑induced pyroptosis via improvements in cell metabolism.Cofilin is associated with cell differentiation; however, to the best of our knowledge, no data have indicated an association between the cofilin 1 pathway and leukemia cell differentiation. The present study investigated the involvement of the cofilin 1 signaling pathway in diallyl disulfide (DADS)‑induced differentiation and the inhibitory effects on the proliferation, migration, and invasion of human leukemia HL‑60 cells. First, it was identified that 8 µM DADS suppressed cell proliferation, migration and invasion, and induced differentiation based on the reduced nitroblue tetrazolium ability and increased CD11b and CD33 expression. DADS significantly downregulated the expression of cofilin 1 and phosphorylated cofilin 1 in HL‑60 leukemia cells. Second, it was verified that silencing cofilin 1 markedly promoted 8 µM DADS‑induced differentiation and the inhibitory effect on cell proliferation and invasion. Overexpression of cofilin 1 obviously suppressed 8 µM DADS‑induced differentiation and the inhibitory effect on cell proliferation and invasion.