Nymannmoore0219

Dysregulated circular RNAs (circRNAs) are involved in the carcinogenesis and progression of multiple human malignancies. Knowledge of circRNAs in glioma (GM) is limited and further study to uncover new therapeutic targets for GM is urgently required. The present study demonstrated that circ‑TOP2A was elevated in GM tissue specimens and cells and that circ‑TOP2A levels indicated an unfavorable clinical prognosis in GM. Functionally, circ‑TOP2A knockdown reduced viability, migration and invasion and triggered apoptosis in LN229 cells. Ectopic expression of circ‑TOP2A aggravated these malignant behaviors in U87MG cells. In terms of mechanism, RNA‑seq was performed to discover the potential targets regulated by circ‑TOP2A. Circ‑TOP2A acted as a competing endogenous RNA to upregulate sushi domain‑containing 2 (SUSD2) expression by sponging microRNA (miR) 346. Rescue assays revealed that the oncogenic function of circ‑TOP2A was partially dependent on its regulation of the miR‑346/SUSD2 axis. In conclusion, the present study identified that circ‑TOP2A promoted GM proliferation and aggressiveness via miR‑346/SUSD2 signaling, which is a potential prognostic biomarker and therapeutic target for GM.Following the publication of the above paper, an interested reader drew to our attention that a number of apparent anomalies existed with the data presented in a couple of the figures in the above paper. Specifically, there appeared to be strikingly similar and duplicated patternings of cells within the cellular images featured in Figs. 3 and 4, which showed apoptotic induction as evaluated by fluorescence microscopy and TEM evaluation of ferruginol‑induced apoptosis in OVCAR‑3 human ovary cancer cells, respectively. Following an internal enquiry, the Editor of Molecular Medicine Reports has been able to verify the claims made by the interested reader; therefore, in view of the potential anomalies that have been identified and owing to a lack of overall confidence in the presented data, the Editorial Board have decided to retract the above paper from the publication. After having passed on this decision to the authors, they were in agreement that the paper should be retracted. The Editor apologizes to the readership of the Journal for any inconvenience caused. [the original article was published in Molecular Medicine Reports 16 7013‑7017, 2017; DOI 10.3892/mmr.2017.7484].The activation of oxidative stress is a primary cause of chondrocyte apoptosis in osteoarthritis (OA). The 78‑kDa glucose‑regulated protein (GRP78)/mammalian target of rapamycin (mTOR) signaling pathway has been demonstrated to be linked with the endoplasmic reticulum (ER) and autophagy. Hydrogen sulfide (H2S) has been reported to exert antioxidant effects. The present study investigated oxidative stress levels via 2',7'‑dichlorofluorescin diacetate and MitoSOX staining, apoptosis rates via flow cytometry and the expression levels of ER stress‑related proteins in GYY4137 (donor of H2S)‑treated chondrocytes (CHs). CHs were isolated from the bilateral hip joints of male rats to examine mitochondrial permeability transition pore opening‑ and mTOR signaling pathway‑related proteins. The results demonstrated that tert‑Butyl hydroperoxide (TBHP) increased CH apoptosis, and treatment with GYY4137 ameliorated TBHP‑mediated the generation of ROS and CH apoptosis. Moreover, TBHP‑treated CHs displayed elevated ER stress sensor expression levels and apoptotic rates; however, the TBHP‑induced protein expression levels were decreased following GYY4137 treatment. In the present study, treatment with either GYY4137 or transfection with GRP78 siRNA both suppressed the activation of p‑P70S6k and p‑mTOR. H2S played an important role in regulating ER stress in TBHP‑stimulated CHs. GYY4137 promoted autophagy, which was accompanied by the inhibition of ER stress. On the whole, the present study demonstrates that TBHP‑induced oxidative stress stimulates ER interactions and CH apoptosis, which are suppressed by exogenous H2S via modulating the GRP78/mTOR signaling pathway.Diabetic nephropathy (DN) is a severe complication of diabetes mellitus and lipid metabolism abnormality serves a key role in the pathogenesis of DN. Sterol regulatory element‑binding protein 1 (SREBP‑1) overexpression mediates aberrant lipid accumulation in renal tubular cells of DN. However, the exact mechanism involved in increased SREBP‑1 has not been fully elucidated. The aim of the present study was to explore the mechanism involved in SREBP‑1 upregulation. Diabetic mice and high glucose‑cultured HKC cells were chosen to detect the expression of FBXW7 and SREBP‑1 using immunohistochemistry, western blotting and PCR. The present study demonstrated that F‑box and WD repeat domain containing 7 (FBXW7) expression was decreased in renal tubular cells of diabetic mice. Moreover, the co‑expression of FBXW7 and SREBP‑1 was observed in renal tubular cells, but not in the glomeruli. Cell Cycle inhibitor High glucose‑induced the downregulation of FBXW7 expression in in vitro cultured HKC cells, which was accompanied by SREBP‑1 upregulation. In addition, overexpression of FBXW7 in HKC cells led to SREBP‑1 downregulation. By contrast, knockdown of FBXW7 caused SREBP‑1 upregulation in HKC cells. It was found that the PI3K/Akt signaling pathway was activated in high glucose‑stimulated HKC cells, and inhibition of PI3K/Akt pathway using LY294002 increased FBXW7 expression and decreased SREBP‑1 expression. Taken together, the present results suggested that FBXW7 mediated high glucose‑induced SREBP‑1 expression in renal tubular cells of DN, under the regulation of the PI3K/Akt signaling pathway.The aim of the present study was to investigate the role of platelet‑derived growth factor (PDGF)‑BB/PDGF receptor (R)‑β signaling in an experimental murine corneal neovascularization (CrNV) model. Experimental CrNV was induced by alkali injury. The intra‑corneal expression of PDGF‑BB was examined using immunohistochemistry. The effect of PDGF‑BB on CrNV was evaluated using immunofluorescence staining. The expression levels of PDGFR‑β in human retinal endothelial cells (HRECs) under normal conditions or following cobalt chloride treatment, which induced hypoxic conditions, was assessed using reverse transcription‑quantitative PCR. The effect of exogenous treatment of PDGF‑BB on the proliferation, migration and tube formation of HRECs under normoxic or hypoxic conditions was evaluated in vitro using Cell Counting Kit‑8, wound healing and 3D Matrigel capillary tube formation assays, respectively. The results indicated that the intra‑corneal expression levels of the proteins of PDGF‑BB and PDGFR‑β were detectable on days 2 and 7 following alkali injury.