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Periodontitis is a chronic inflammatory disease caused by the gradual breakdown of tissues surrounding the teeth due to various factors. The disease has been frequently noted in dental outpatients for a number of years. Improvements are required to current diagnostic methods, which have limitations in assessing the condition and progression of periodontitis. The development of diagnostic biomarkers for periodontitis to increase the sensitivity and accuracy of diagnosis is important for the management of periodontitis. In the present study, whole gingival crevicular fluid (GCF) from patients with periodontitis and healthy individuals was characterized via liquid chromatography with tandem mass spectrometry. Label‑free quantification was used to identify the differentially abundant protein biomarkers. A total of 1,295 proteins were identified from the whole GCF of patients with periodontitis and healthy individuals via proteomic analysis. When analyzing biological processes, 'metabolic process' and 'cell organization and biogenes' were identified to play important roles in GCF under periodontitis conditions according to Gene Ontology. When analyzing molecular functions, 'catalytic activity' and 'protein binding' were the terms most enriched with differentially abundant proteins under periodontitis conditions. Galectin‑10 (Gal‑10) was one of the most upregulated proteins in the GCF of patients with periodontitis. The levels of prostaglandin E2 were increased in oral keratinocytes and gingival fibroblasts treated with recombinant (r)Gal‑10. The levels of interleukin‑8, matrix metalloproteinase 9 and C‑reactive protein were increased in the conditioned media (CM) of rGal‑10‑treated gingival fibroblasts. In addition, the CM of rGal‑10‑treated gingival fibroblasts induced osteoclast differentiation. These results suggested that Gal‑10 expression was increased in the GCF of patients with periodontitis and contributed to the process of osteoclastogenesis. Therefore, Gal‑10 may be a candidate biomarker for periodontitis.Colorectal cancer (CRC) is the third most common malignant tumor in humans. Chemotherapy is used for the treatment of CRC. However, the effect of chemotherapy remains unsatisfactory due to drug resistance. Growing evidence has shown that the presence of highly metastatic tumor stem cells, regulation of non‑coding RNAs and the tumor microenvironment contributes to drug resistance mechanisms in CRC. Wnt/β‑catenin signaling mediates the chemoresistance of CRC in these three aspects. Therefore, the present study analyzed the abundant evidence of the contribution of Wnt/β‑catenin signaling to the development of drug resistance in CRC and discussed its possible role in improving the chemosensitivity of CRC, which may provide guidelines for its clinical treatment.Age‑related renal diseases, which account for various progressive renal disorders associated with cellular and organismal senescence, are becoming a substantial public health burden. However, their aetiologies are complicated and their pathogeneses remain poorly understood. Telomeres and telomerase are known to be essential for maintaining the integrity and stability of eukaryotic genomes and serve crucial roles in numerous related signalling pathways that activate renal functions, such as repair and regeneration. Previous studies have reported that telomere dysfunction served a role in various types of age‑related kidney disease through various different molecular pathways. The present review aimed to summarise the current knowledge of the association between telomeres and ageing‑related kidney diseases and explored the contribution of dysfunctional telomeres to these diseases. The findings may help to provide novel strategies for treating patients with renal disease.The poor prognosis of non‑small cell lung cancer (NSCLC) is related to epithelial‑mesenchymal transition (EMT). Recent studies demonstrated that non‑coding RNA activated by DNA damage (NORAD) displays a carcinogenic effect and targets microRNA (miR)‑422a, which may be involved in tumor cell migration and invasion. The aim of the present study was to investigate the effect of NORAD on NSCLC cell EMT and the underlying mechanism. Reverse transcription‑quantitative PCR and western blotting were performed to detect the expression levels of long non‑coding RNAs, miRNAs and mRNAs. Cell viability, migration and invasion were detected by conducting Cell Counting Kit‑8, wound healing and Transwell assays, respectively. The target of NORAD was predicted using starBase and further confirmed by conducting a dual‑luciferase reporter assay. The results indicated that NORAD expression was significantly increased in lung cancer tissues and cells compared with adjacent healthy tissues and cells. Compared with the control groups, NORAD overexpression promoted SK‑MES‑1 cell viability, migration and invasion, whereas NORAD knockdown resulted in the opposite effects in A549 cells. Moreover, miR‑422a, which was predicted to be a target of NORAD, displayed lower expression levels in lung cancer tissues compared with adjacent healthy tissues. In addition, miR‑422a overexpression partially reversed NORAD overexpression‑induced increases in SK‑MES‑1 cell viability, migration, invasion and EMT. In addition, miR‑422a knockdown partially reversed the effects of NORAD knockdown. The present study suggested that NORAD regulated lung cancer cell EMT by regulating the expression of miR‑422a, providing a potential therapeutic target for the intervention of the development of NSCLC.Endoplasmic reticulum stress (ERS) contributes to the pathogenesis of myocardial ischemia/reperfusion injury and myocardial infarction (MI). Tat-beclin 1 purchase Long non-coding RNAs (lncRNAs) serve an important role in cardiovascular diseases, and lncRNA discrimination antagonizing non-protein coding RNA (Dancr) alleviates cardiomyocyte damage. microRNA (miR)-6324 was upregulated in MI model rats and was predicted to bind to Dancr. The present study aimed to investigate the role of Dancr in ERS-induced cardiomyocytes and the potential underlying mechanisms. Tunicamycin (Tm) was used to induce ERS. Cell viability, apoptosis and levels of associated proteins, ERS and autophagy in Dancr-overexpression H9C2 cells and miR-6234 mimic-transfected H9C2 cells were assessed using Cell Counting Kit-8, TUNEL staining and western blot assay, respectively. The results suggested that Dancr expression levels and cell viability were downregulated by Tm in a concentration-dependent manner compared with the control group. Tm induced apoptosis, ERS and autophagy, as indicated by an increased ratio of apoptotic cells, increased expression levels of Bax, cleaved (c)-caspase-3/9, glucose-regulated protein 78 kDa (GRP78), phosphorylated (p)-inositol-requiring enzyme-1α (IRE1α), spliced X-box-binding protein 1 (Xbp1s), IRE1α, activating transcription factor (ATF)6, ATF4, Beclin 1 and microtubule associated protein 1 light chain 3α (LC3)II/I, and decreased expression levels of Bcl-2, unspliced Xbp1 (Xbp1u) and p62 in the Tm group compared with the control group.
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