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Renal autotransplantation to treat kidney artery aneurysm.
MicroRNAs (miRs), which act as crucial regulators of oncogenes and tumor suppressors, have been confirmed to play a significant role in the initiation and progression of various malignancies, including glioma. The present study analyzed the expression and roles of miR‑422a in glioma, and reverse transcription‑quantitative PCR confirmed that miR‑422a expression was significantly lower in glioblastoma multiforme (GBM) samples and cell lines compared with the low‑grade glioma samples and the H4 cell line, respectively. miR‑422a overexpression suppressed proliferation and invasion, and induced apoptosis in LN229 and U87 cell lines. Luciferase reporter assay, western blotting and RNA immunoprecipitation analysis revealed that ribophorin II (RPN2) is a direct functional target of miR‑422a. Additionally, the overexpression of RPN2 partially reversed the miR‑422a‑mediated inhibitory effect on the malignant phenotype. Mechanistic investigation demonstrated that the upregulation of miR‑422a inhibited β‑catenin/transcription factor 4 transcriptional activity, at least partially through RPN2, as indicated by in vitro and in vivo experiments. Furthermore, RPN2 expression was inversely correlated with miR‑422a expression in GBM specimens and predicted patient survival in the Chinese Glioma Genome Atlas, UALCAN, Gene Expression Profiling Interactive Analysis databases. In conclusion, the present data reveal a new miR‑422a/RPN2/Wnt/β‑catenin signaling axis that plays critical roles in glioma tumorigenesis, and it represents a potential therapeutic target for GBM.Oxidized low‑density lipoprotein (ox‑LDL)‑induced endothelial cell (EC) injury is a risk factor for atherosclerosis. Therefore, the present study aimed to investigate the effects of insulin‑receptor substrate 1 (IRS‑1) on injury to ox‑LDL‑exposed ECs. For this purpose, thoracic aorta tissues were isolated from rats and cultured to obtain ECs, which were then identified using immunohistochemical staining. IRS‑1 overexpression plasmid (pcDNA3.1‑IRS‑1) and IRS‑1‑small interfering RNA were synthesized and transfected into ECs pre‑exposed to ox‑LDL. MTT and TUNEL assays were performed to evaluate the cell proliferative activity and apoptosis. Intracellular reactive oxygen species (ROS) production was determined by a flow cytometry assay. Reverse transcription‑quantitative PCR was conducted to measure the peroxisome proliferator‑activated receptor gamma co‑activator 1 alpha (Ppargcla), phosphoenolpyruvate carboxykinase 1 (Pck1) and glucose‑6‑phosphatase catalytic subunit (G6pc) gene transcription levels. Western blment (P less then 0.05). Moreover, IRS‑1 promoted the phosphorylation of Akt in the EC models of ox‑LDL‑induced atherosclerosis. IRS‑1 also significantly suppressed the transcription of atherosclerosis‑associated genes in ox‑LDL‑exposed ECs compared with ECs without IRS‑1 treatment (P less then 0.05). Furthermore, TAE684 concentration ‑1 significantly increased the cytoplasmic localization of p‑FoxO1 in EC models of ox‑LDL‑induced atherosclerosis. On the whole, the findings of the present study demonstrate that IRS‑1 exerts protective effects in an EC model of ox‑LDL‑induced atherosclerosis by inhibiting ER stress/oxidative stress‑mediated apoptosis and activating the Akt/FoxO1 signaling pathway.Curcumin is the main component of the Chinese herbal plant turmeric, which has been demonstrated to possess antitumor and other pharmacological properties. The aim of the present study was to investigate the effects of curcumin on the viability, migration and apoptosis of human colorectal carcinoma HCT‑116 cells, and to explore the underlying molecular mechanisms. In addition, it was investigated whether the antitumor effect of curcumin on HCT‑116 cells could match that of the chemotherapeutic drug 5‑fluorouracil (5‑FU). HCT‑116 cells were treated with curcumin (10, 20 and 30 µM) and 5‑FU (500 µM), and cell viability and proliferation were detected by Cell Counting Kit‑8 and colony formation assays, respectively. The migration and invasion of treated cells were determined using Transwell and carboxyfluorescein succinimidyl amino ester fluorescent labeling assays. Cell cycle distribution and apoptosis rates were detected by flow cytometry. Furthermore, cell morphology changes associated with apoptosis were obse‑dependent manner. By contrast, the expression of migration‑associated proteins, including MMP‑9, NF‑κB and claudin‑3, was downregulated with increasing curcumin concentrations. These data suggested that the inhibitory effect of curcumin on HCT‑116 cells may match that of 5‑FU. Therefore, curcumin induced cell apoptosis and inhibited tumor cell metastasis by regulating the NF‑κB signaling pathway, and its therapeutic effect may be comparable to that of 5‑FU.Treatment‑resistant schizophrenia (TRS) is a common phenotype of schizophrenia that places a considerable burden on patients as well as on society. TRS is known for its tendency to relapse and uncontrollable nature, with a poor response to antipsychotics other than clozapine. Therefore, it is urgent to identify objective biological markers, so as to guide its treatment and associated clinical work. #link# In the present study, the peripheral blood mononuclear cells (PBMCs) of patients with TRS and a healthy control group, which were gender‑, age‑ and ethnicity‑matched, were subjected to microRNA (miRNA/miR) sequencing to screen out the top three miRNAs with the highest fold change values. These were then validated in the TRS (n=34) and healthy control (n=31) groups by reverse transcription‑quantitative PCR. For two of the top three miRNAs, the PCR results were in accordance with the sequencing result (P less then 0.01), while the third miRNA exhibited the opposite trend (P less then 0.01). To elucidate the functions of these two miRNAs, Homo sapiens (hsa)‑miR‑218‑5p and hsa‑miR‑1262 and their regulatory network, target gene prediction was first performed using online TargetScan and Diana‑micro T software. Bioinformatics analysis was then performed using functional enrichment analysis to determine the Gene Ontology terms in the category biological process and the Kyoto Encyclopedia of Genes and Genomes pathways. It was revealed that these target genes were markedly associated with the nervous system and brain function, and it was obvious that the differentially expressed miRNAs most likely participated in the pathogenesis of TRS. A receiver operating characteristic curve was generated to confirm the distinct diagnostic value of these two miRNAs. It was concluded that aberrantly expressed miRNAs in PMBCs may be implicated in the pathogenesis of TRS and may serve as specific peripheral blood‑based biomarkers for the early diagnosis of TRS.
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