Notes

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, rescued the effects of si‑DUXAP8 on cell proliferation and apoptosis. The present study was the first to identify DUXAP8 as a novel upregulated lncRNA in PTC, and provided new insights in understanding the effect of the lncRNA‑miRNA‑mRNA network in PTC.Oral tongue squamous cell carcinoma (OTSCC) is one of the most aggressive pathological types of head and neck squamous cell carcinoma, and presents with rapid local invasion and metastasis. The present study confirmed that the long non‑coding (lnc) RNA MIR4713HG was markedly upregulated in both OTSCC tissues and cell lines and associated with poor survival. The present study performed a series of experiments to investigate the impact of MIR4713HG on OTSCC and revealed that upregulation of MIR4713HG had a crucial role in promoting cell proliferation and metastasis of OTSCC cell lines both in vitro and in vivo. By applying bioinformatics analyses, micro RNA let‑7c‑5p was observed to physically bind with MIR4713HG, and the knockdown of let‑7c‑5p could counteract the influence of MIR4713HG on OTSCC. Furthermore, the present study demonstrated that let‑7c‑5p performed its regulating role in OTSCC via affecting the expression level of transmembrane channel like 7 (TMC7). In conclusion, the present study demonstrated that lncRNA MIR4713HG acted as a pro‑tumor factor facilitating cell proliferation and metastasis of OTSCC via affecting the let‑7c‑5p/TMC7 signaling pathway, which presents as a promising therapeutic target in OTSCC.The present study aimed to elucidate the biological function of circular RNAs (circRNA) 0074027 in colorectal cancer (CRC). The expression of circRNA‑0074027 in CRC tissues and cells was determined by reverse transcription‑quantitative PCR. The in vitro experiments, including Cell Counting Kit‑8 (CCK‑8) assay, 5‑Ethynyl‑2'‑deoxyuridine assay, flow cytometry and Transwell assay, were applied to evaluate cell proliferation, apoptosis and metastasis ability respectively following downregulation of circRNA‑0074027. The correlation between circRNA‑0074027 and micro (mi)RNA‑525‑3p was determined via dual‑luciferase reporter assay. Finally, western blotting was used to explore the possible regulatory mechanism. CircRNA‑0074027 was upregulated in CRC tissues, while miR‑525‑3p expression was reduced. In addition, patients with CRC and circRNA‑0074027 overexpression were more likely to have low tumor differentiation, lymph node metastasis and advanced TMN stage. Deletion of circRNA‑0074027 could suppress cell proliferation and metastasis through up-regulating p53 expression and forbidding epithelial‑mesenchymal transition signaling pathway. The addition of miRNA‑525‑3p inhibitors could reverse the anti‑tumor effects induced by the deletion of circRNA‑0074027. The downregulation of cirRNA_0074027 inhibited tumor progression via sponging miR‑525‑3p, which could be a promising treatment bio‑marker for CRC.Respiratory disease is a common disease with a high incidence worldwide, which is a serious threat to human health, and is considered a societal and economic burden. The application of nanotechnology in drug delivery systems has created new treatments for respiratory diseases. Within this context, the present review systematically introduced the physicochemical properties of nanoparticles (NPs); reviewed the current research status of different nanocarriers in the treatment of respiratory diseases, including liposomes, solid lipid nanocarriers, polymeric nanocarriers, dendrimers, inorganic nanocarriers and protein nanocarriers; and discussed the main advantages and limitations of therapeutic nanomedicine in this field. The application of nanotechnology overcomes drug inherent deficiencies to a certain extent, and provides unlimited potential for the development of drugs to treat respiratory diseases. However, most of the related research work is in the preclinical experimental stage and safety assessment is still a challenging task. Future studies are needed to focus on the performance modification, molecular mechanism and potential toxicity of therapeutic nanomedicine.Glycyrrhizin (GA) is the most essential active ingredient in licorice root, and has a wide range of biological and pharmacological activities. The present study aimed to conduct a detailed analysis of the effects of GA on liver cancer (LC) cell proliferation and the Warburg effect. Hexokinase‑2 (HK2) is a glycolytic enzyme that catalyzes the Warburg effect. To this end, the LC HepG2 cell line was transfected with small interfering RNA‑HK2 or pCDNA3.1‑HK2, followed by GA treatment. A Cell Counting Kit‑8 assay and EdU staining were employed to evaluate the proliferation rate of LC cells. The expression levels of HK2 and the phosphorylation level of AKT were measured by reverse transcription‑quantitative PCR and western blotting, respectively. Furthermore, the glucose uptake capacity and lactic acid content were assessed by kits, and the glycolysis level was evaluated by assessing the extracellular acidification rate (ECAR) and the oxygen consumption rate (OCR). A pronounced increase in the OCR, and decreases in the cell proliferation, glucose uptake capacity, lactic acid content, ECAR and HK2 expression were detected in LC cells subjected to GA treatment or HK2‑knockdown. Conversely, overexpression of HK2 reversed these trends, indicating that glycyrrhizin may inhibit LC cell proliferation and the Warburg effect through suppression of HK2. In addition, it was revealed that the PI3K/AKT signaling pathway was associated with LC cell proliferation and the Warburg effect; notably, treatment of LC cells with the AKT agonist SC79 induced elevation of the ECAR, cell proliferation, glucose uptake capacity, lactic acid content, phosphorylated‑AKT and HK2 expression, and suppressed the OCR. In conclusion, GA may inhibit the Warburg effect and cell proliferation in LC by suppressing HK2 through blockade of the PI3K/AKT signaling pathway.Lipopolysaccharide (LPS) from oral pathogenic bacteria is an important factor leading to alveolar bone absorption and the implant failure. The present study aimed to evaluate the modulation of berberine hydrochloride (BBR) on the LPS-mediated osteogenesis and adipogenesis imbalance in rat bone marrow-derived mesenchymal stem cells (BMSCs). Cell viability, osteoblastic and adipogenic differentiation levels were measured using the Cell Counting Kit-8 assay, alkaline phosphatase (ALP) staining and content assay, and oil red O staining, respectively. Reverse transcription-quantitative PCR and immunoblotting were used to detect the related gene and protein expression levels. In undifferentiated cells, BBR increased the mRNA expression levels of the osteoblastic genes (Alp, RUNX family transcription factor 2, osteocalcin and secreted phosphoprotein 1) but not the adipogenic genes (fatty acid binding protein 4, Adipsin and peroxisome proliferator-activated receptorγ). LPS-induced osteoblastic gene downregulation, adipogenic gene enhancement and NF-κB activation were reversed by BBR treatment. In osteoblastic differentiated cells, decreased ALP production by LPS treatment was recovered with BBR co-incubation. In adipogenic differentiated cells, LPS-mediated lipid accumulation was decreased by BBR administration. The mRNA expression levels of the pro-inflammatory factors (MCP-1, TNF-α, IL-6 and IL-1β) were increased by LPS under both adipogenic and osteoblastic conditions, which were effectively ameliorated by BBR. The actions of BBR were attenuated by compound C, suggesting that the role of BBR may be partly due to AMP-activated protein kinase activation. The results demonstrated notable pro-osteogenic and anti-adipogenic actions of BBR in a LPS-stimulated inflammatory environment. This indicated a potential role of BBR for bacterial infected-related peri-implantitis medication.Myocardial ischemia‑reperfusion injury (MIRI) is a severe injury to the ischemic myocardium following the recovery of blood flow. Currently, there is no effective treatment for MIRI in clinical practice. Over the past two decades, biological studies of hypoxia and hypoxia‑inducible factor‑1α (HIF‑1α) have notably improved understanding of oxygen homeostasis. HIF‑1α is an oxygen‑sensitive transcription factor that mediates adaptive metabolic responses to hypoxia and serves a pivotal role in MIRI. In particular, previous studies have demonstrated that HIF‑1α improves mitochondrial function, decreases cellular oxidative stress, activates cardioprotective signaling pathways and downstream protective genes and interacts with non‑coding RNAs. The present review summarizes the roles and associated mechanisms of action of HIF‑1α in MIRI. In addition, HIF‑1α‑associated MIRI intervention, including natural compounds, exosomes, ischemic preconditioning and ischemic post‑processing are presented. The present review provides evidence for the roles of HIF‑1α activation in MIRI and supports its use as a therapeutic target.Long non‑coding RNAs are associated with cancer progression. Long intergenic non‑protein coding RNA (linc)‑regulator of reprogramming (ROR) enhances tumor development in hepatocellular carcinoma (HCC). However, the effect of chemoresistance and its underlying mechanisms in HCC are not completely understood. The present study aimed to identify the effect of ROR on sensitivity to doxorubicin (DOX) in HCC cells. In the present study, Cell Counting Kit‑8 and EdU assays were performed to assess cell viability and proliferation, respectively. In addition, E‑cadherin and vimentin protein expression levels were assessed via western blotting and immunofluorescence.The results of the present study demonstrated that HCC cells with high linc‑ROR expression levels were more resistant to DOX, and linc‑ROR knockdown increased HCC cell DOX sensitivity compared with the control group. The results indicated that compared with the NC siRNA group, linc‑ROR knockdown notably suppressed epithelial‑mesenchymal transition by downregulating twist family bHLH transcription factor 1 (TWIST1) expression. TWIST1 knockdown displayed a similar effect on HCC cell DOX sensitivity to linc‑ROR knockdown. Moreover, linc‑ROR knockdown‑induced HCC cell DOX sensitivity was inhibited by TWIST1 overexpression. The present study provided evidence that linc‑ROR promoted HCC resistance to DOX by inducing EMT via interacting with TWIST1. Therefore, linc‑ROR might serve as a therapeutic target for reducing DOX resistance in HCC.Heart transplantation is widely used for the treatment of several heart diseases. Regulatory B cells (Breg cells) serve a critical role in immune tolerance. However, the role of Breg cells in immune tolerance in the context of allogeneic heart transplantation remains poorly understood. Selleck Veliparib The present study aimed to explore the effect of histone deacetylase (HDAC) inhibitor trichostatin A (TSA)‑regulated Breg on the regulation of immune tolerance in heart transplantation. By constructing anallogeneic heart transplantation mouse model, and performing flow cytometry, reverse transcription‑quantitative PCR, western blotting and carboxyfluorescein succinimidyl esterstaining assays, TSA‑regulated Breg cells and their effects on immune tolerance in heart transplantation were evaluated. The results demonstrated that TSA increased the frequency of CD19+CD5+CD1dhigh Breg cells both in vitro and in vivo. Moreover, TSA treatment increased the frequency of IL‑10 and TGF‑β‑producing CD19+CD5+CD1dhigh Breg cells, and IL‑10 and TGF‑β levels in vitro and in vivo.
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