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Clear cell renal cell carcinoma (CCRCC) with sarcomatoid differentiation (CCRCCS) displays invasive behavior, poor prognosis, and poor therapeutic response. The present study was aimed to gain new insights into the molecular mechanisms of sarcomatoid transformation, and identify new prognostic and therapeutic targets for CCRCCS. Whole exome sequencing was performed on matched carcinomatous and sarcomatoid elements from five specimens with CCRCCS. A non‑synonymous single‑nucleotide polymorphism (SNP) of cadherin 23 (CDH23) was further studied through Sanger sequencing in expanded 40 specimens with CCRCCS and 50 specimens with CCRCC. Carcinomatous and sarcomatoid elements shared most somatic single‑nucleotide variants (SSNVs) as revealed through whole exome sequencing. Sarcomatoid element had higher overall SSNVs than carcinomatous element. A highly frequent mutation of CDH23 (rs3802711) was observed in CCRCCS that resulted in an alteration in the highly conserved calcium‑binding site in the three‑dimensional ( identified.Laryngeal carcinoma (LCC) is a common malignant tumor with low radiosensitivity and generally poor response rates. The ubiquitin protein ligase E3 component n‑recognin 5 (UBR5) has prognostic implications in several neoplasms; however, its role in LCC and radiotherapy sensitivity remains unknown. Immunohistochemistry and bioinformatics analyses were performed to measure UBR5 protein and mRNA expression in LCC and adjacent non‑tumor tissues. The gene and protein expression of UBR5 in LCC and HuLa‑PC cell lines were measured using quantitative PCR and western blot analyses. Following transfection with small interfering RNA or UBR5 overexpression plasmid in LCC cells, the proliferation, cell cycle distribution, invasion, migration and radiosensitivity of LCC cells were analyzed. UBR5‑related lncRNA, targeted miRNA and protein‑protein interaction networks were analyzed using bioinformatics. Finally, the expression of the p38/mitogen‑activated protein kinase (MAPK) pathway was evaluated following UBR5 silencing in cell proliferation and sensitivity to radiotherapy in LCC via the p38/MAPK pathway, thereby highlighting its possible value for the development of new therapeutic strategies and targets for the treatment of this disease.Colorectal carcinoma (CRC) is a major type of malignancy worldwide. Ellagic acid (EA), a natural phenolic constituent, has been shown to exhibit anticancer effects. In our previous study, it was shown that EA inhibited proliferation of CRC cells. Additionally, microarray analysis revealed 4,738 differentially expressed genes (DEGs) which were associated with multiple cellular events, including cell growth, apoptosis and angiogenesis. However, the associated pathways had not been validated. In the present study, it was shown that EA induced G0/G1 cell cycle arrest in HCT‑116 cells, and increased apoptosis. Furthermore, DEGs identified by cDNA microarray analysis were investigated, and showed changes in five genes which were associated with the TGF‑β1/Smad3 signaling pathway. TGF‑β1 small interfering RNA and SIS3, a Smad3 inhibitor, were used to assess the role of TGF‑β1 and Smad3, respectively, and it was shown that the they reduced the effects of EA on HCT‑116 CRC cells. In addition, the expression patterns of downstream DEGs of the TGF‑β1/Smad3 pathway were altered. Thus, this pathway may underlie the molecular mechanism by which EA exhibits its effects in vitro in CRC cells. Accordingly, targeting the TGF‑β1/Smad3 pathway with anticancer agents such as EA may be potentially used to treat CRC.Abnormal microRNA (miRNA) expression has been implicated in spinal cord injury (SCI), but the underlying mechanisms are poorly understood. To observe the effect of electroacupuncture (EA) on miRNA expression profiles in SCI rats and investigate the potential mechanisms involved in this process, Sprague‑Dawley rats were divided into sham, SCI and SCI+EA groups (n=6 each). Basso, Beattie and Bresnahan (BBB) scoring and hematoxylin‑eosin staining of cortical tissues were used to evaluate spinal cord recovery with EA treatment 21 days post‑surgery across the three groups. To investigate miRNA expression profiles, 6 Sprague‑Dawley rats were randomly divided into SCI and SCI+EA groups (n=3 in each group) and examined using next‑generation sequencing. Integrated miRNA‑mRNA‑pathway network analysis was performed to elucidate the interaction network of the candidate miRNAs, their target genes and the involved pathways. Behavioral scores suggested that hindlimb motor functions improved with EA treatments. Apoptotic indices were lower in the SCI+EA group compared with the SCI group. It was also observed that 168 miRNAs were differentially expressed between the SCI and SCI+EA groups, with 29 upregulated and 139 downregulated miRNAs in the SCI+EA group. Changes in miRNA expression are involved in SCI physiopathology, including inflammation and apoptosis. Reverse transcription‑quantitative PCR measurement of the five candidate miRNAs, namely rno‑miR‑219a‑5p, rno‑miR‑486, rno‑miR‑136‑5p, rno‑miR‑128‑3p, and rno‑miR‑7b, was consistent with RNA sequencing data. Integrated miRNA‑mRNA‑pathway analysis suggested that the MAPK, Wnt and NF‑κB signaling pathways were involved in EA‑mediated recovery from SCI. The present study evaluated the miRNA expression profiles involved in EA‑treated SCI rats and demonstrated the potential mechanism and functional role of miRNAs in SCI in rats.Dihydroartemisinin (DHA) is a semisynthetic derivative of artemisinin, which has been found to exhibit a broad range of biological activities, excluding antimalarial effects; however its effects on the gut microbiota remain poorly understood. SC79 The present study aimed to investigate the effects of DHA on the gut microbiome in mice and to determine its potential biological and pharmaceutical activities through its alteration of the gut microbiota. Serum glucose, triglyceride (TG), total cholesterol, lipopolysaccharide, high density lipoprotein‑cholesterol, low density lipoprotein‑cholesterol, alanine aminotransferase and aspartate aminotransferase levels in mice treated with DHA were analyzed using the corresponding detection kits. In addition, hematoxylin and eosin staining was performed to determine the pathological effects of DHA on the liver, kidney and intestinal tissues of mice, and the effects of DHA on the gut microbiome were analyzed using 16S ribosomal (r)DNA gene analysis. The results demonstrated that the TG serum levels of mice treated with DHA were significantly decreased compared with the control group.
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