OBJECTIVE Gastric cancer (GC) is one of the most ordinary malignant tumors. Recent studies have revealed that circular RNAs (circRNAs) play an important role in the progression of tumorigenesis. In this research, circ-SMAD7 was selected to identify how it functions in the progression of GC. PATIENTS AND METHODS Circ-SMAD7 expression in paired GC patients' tissue samples and cell lines was detected by Real Time-quantitative Polymerase Chain Reaction (RT-qPCR). The role of circ-SMAD7 in the metastasis of GC was detected through wound healing assay and transwell assay. Western blot assay and RT-qPCR were used to discover the function of circ-SMAD7 in epithelial-to-mesenchymal transition (EMT) process. Furthermore, tumor metastasis assay was also performed in vivo. RESULTS In this study, RT-qPCR results showed that circ-SMAD7 expression was significantly lower in GC tissues compared to that in adjacent ones. Cell migration and invasion of GC were inhibited via upregulation of circ-SMAD7.  https://www.selleckchem.com/products/ly333531.html  Moreover, the results of further experiments revealed that the EMT-related proteins were regulated via upregulation of circ-SMAD7 in GC. Furthermore, tumor metastasis of GC was inhibited via upregulation of circ-SMAD7 in nude mice. CONCLUSIONS These results indicate that upregulation of circ-SMAD7 inhibits GC cell migration and invasion via reversing the EMT process.OBJECTIVE LncRNA nuclear enriched abundant transcript 1 (NEAT1) has been reported to play an oncogenic role in the occurrence and development of diabetic nephropathy (DN). The aim of our study was to investigate the potential mechanism by which NEAT1 facilitates the progression of DN. PATIENTS AND METHODS Quantitative Real-time polymerase chain reaction (qRT-PCR) was carried out to determine the abundance of NEAT1, kidney injury molecule-1 (KIM-1), neutrophil gelatinase-associated lipocalin (NGAL), proliferating cell nuclear antigen (PCNA), Cyclin D1, P38, apoptosis signal-regulating kinase 1 (ASK1), Fibronectin, α smooth muscle actin (α-SMA) and miR-23c in the serum of DN patients, normal patients and mouse mesangial cells (MMCs). Cell proliferation was assessed by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), qRT-PCR and Western blot assays. Flow cytometry and Western blot were applied to measure apoptosis of MMCs. Cell fibrosis and epithelial-to-mesenchymal transition (EMT) were analyzed by qRT-PCR and Western blot. The binding sites between miR-23c and NEAT1 were predicted by starBase bioinformatics software, and the relationship was verified by dual-luciferase reporter assay. RESULTS The enrichment of NEAT1 was elevated in the serum of DN patients and MMCs induced by high concentration of glucose. NEAT1 overexpression accelerated proliferation, fibrosis and EMT and restrained apoptosis of MMCs induced by high concentration of glucose. MiR-23c bound to NEAT1, and the inhibition of miR-23c counteracted the suppressive effect of NEAT1 depletion on proliferation, fibrosis and EMT of MMCs induced by high concentration glucose. CONCLUSIONS LncRNA NEAT1 promoted proliferation, fibrosis and EMT while impeded apoptosis of MMCs through sponging miR-23c. LncRNA NEAT1 and miR-23c might be underlying therapeutic targets for the treatment of DN.OBJECTIVE Diabetic nephropathy (DN) is one of the most representative diabetic microangiopathy complications. So far, there have been no satisfactory therapeutic strategies, and the injection of stem cells provides a target for DN therapy. PATIENTS AND METHODS Urine-derived stem cells (USCs) were obtained from 9 healthy men. 24 mice were randomly and equally divided into control group, DN model group, DN+hUSC group (treated with USCs for 3 times). Hematoxylin-eosin (HE) and Masson staining were used to detect histological changes of kidney injury. Creatinine and blood urea nitrogen (BUN) were measured to assess renal function. Besides, myofibroblast accumulation, macrophage infiltration, cell proliferation, and oxidative stress were detected by immunohistochemical analysis. RESULTS Compared with DN model group, DN+hUSC group showed lower function loss, cell infiltration, and oxidative stress, as well as less renal fibrosis, histological damage, and cell proliferation. CONCLUSIONS USC can alleviate inflammation and oxidative stress, reduce renal interstitial fibrosis, improve renal tissue structure and protect renal function through paracrine effect.OBJECTIVE Glioma is a common aggressive cancer and a major public health problem worldwide, with high incidence, recurrence, and mortality. Circular RNA (circRNA) has been reported to be involved in glioma, but the role of circ_0079593 in glioma is still unclear. MATERIALS AND METHODS The real-time quantitative polymerase chain reaction (RT-qPCR) was performed to quantify the expression levels of circ_0079593, miR-499a-5p, and karyopherin alpha 2 (KPNA2) in glioma tissues or cells. The protein expression level of KPNA2 was assessed by Western blot. 3-(4, 5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazol-3-ium bromide (MTT), flow cytometry, and transwell assays were conducted to evaluate proliferation, apoptosis, migration and invasion of glioma cells, respectively. The relationship between miR-499a-5p and circ_0079593 or KPNA2 was analyzed by bioinformatics database and confirmed by Dual-Luciferase reporter analyses, respectively. The effects of circ_0079593 silencing in vivo were measured by a xenograft experiment. RESULTS Circ_0079593 and KPNA2 were elevated in glioma tissues and cells. Loss-of functional experiments revealed that knockdown of circ_0079593 hampered the progression of glioma by repressing proliferation, motility and inducing apoptosis in vitro and declining tumor growth in vivo. Similarly, suppression of KPNA2 impeded the process of glioma by inhibiting proliferation, motility and increasing apoptosis. MiR-499a-5p, interacting with KPNA2, was a target gene of circ_0079593. In addition, overexpression of KPNA2 could reverse the effects of circ_0079593 knockdown on proliferation, apoptosis, migration and invasion of glioma cells. Mechanistically, circ_0079593 mediated proliferation, motility and apoptosis of glioma cells by regulating KPNA2 expression via sponging miR-499a-5p. CONCLUSIONS Circ_0079593 stimulated the pathological process of glioma via acting as competing endogenous RNA to sponge miR-499a-5p.