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Long non-coding RNAs (lncRNAs) have been demonstrated to serve vital roles in renal cell carcinoma (RCC) development. Gastric carcinoma high expressed transcript 1 (GHET1) regulates numerous biological processes in cancer cells. However, the biological role of GHET1 in RCC has not yet been identified. This study aimed to investigate the role of GHET1 in RCC. In the present study, the expression of GHET1 in RCC tissues and the 786-O, A498 and 293 cell lines was assessed by reverse transcription-quantitative polymerase chain reaction. Cell Counting Kit-8, colony formation and cell scratch assays were used to determine the effects of GHET1 on tumorigenesis. Western blotting was performed to examine the effect of GHET1 on epithelial-mesenchymal transition (EMT) in RCC cells. GHET1 expression was significantly increased in the RCC samples in comparison with adjacent tissues. High expression levels of GHET1 were associated with distant metastasis and clinical stage severity, thus, high GHET1 expression may serve as a predictor for a poor prognosis. In addition, RCC cells presented higher GHET1 mRNA and protein expression levels compared with in 293 cells. Furthermore, silencing GHET1 suppressed cell growth, weakened cell migration and inhibited EMT of RCC cells in vitro. In conclusion, the present study suggested that GHET1 may be considered a therapeutic target for the treatment or prevention of RCC. [ABSTRACT FROM AUTHOR]

Clostridium butyricum (CB), a probiotic, is a gram-positive obligate anaerobic bacillus with acid and heat resistant properties. Previous studies have reported that CB has beneficial effects in intestinal diseases and regulates intestinal function. The aim of the present study was to investigate the protective effects and mechanisms of CB on the intestinal barrier function. Mice were randomly divided into three experimental groups (n=15 mice/group), including control, dextran sodium sulfate (DSS) and DSS + CB. In the DSS and DSS + CB groups colitis was induced with 3% DSS dissolved in drinking water for 7 days. DSS + CB group mice were co-treated daily with 200 µl (2x108 CFU) CB solution via gavage. The intestinal mucosal barrier function in mice was assessed by measuring FITC-labeled 4-kDa dextran (molecular weight, 4,000 Da) flux and by analyzing the expression of tight junction (TJ)-related proteins using western blot analysis. In addition, the secretion levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6, IL-10 and IL-13, and the concentration of malondialdehyde, glutathione and superoxide dismutase were detected using ELISAs to determine inflammation and oxidative stress, respectively. The activation status of the Akt/mTOR signaling pathway was also investigated using western blot analysis. The results demonstrated that, in mice with DSS-induced colitis treatment, co-treatment with CB attenuated colitis symptoms and intestinal permeability, increased the expression levels of TJ-related proteins, decreased TNF-α, IL-1β and IL-13 secretion levels but increased those of IL-10, and reduced oxidative stress. Additionally, CB elevated the phosphorylation of Akt, mTOR and p70 ribosomal protein S6 kinase. Collectively, the present results indicated that CB protected intestinal barrier function and decreased intestinal mucosal permeability via upregulating the expression levels of TJ-related proteins in a mouse model of DSS-induced colitis. Moreover, the results suggested that the effects of CB could be mediated by the Akt/mTOR signaling pathway. [ABSTRACT FROM AUTHOR]

Highlights from the article: After the publication of the above paper, the authors requested a change in the order of a pair of the authors listed on the paper; essentially, the placement of the second- and third-listed authors on the paper has been reversed, and so Xin Liu is now the second named author, and Qiang Chen is the third author. Furthermore, for the record, the authors who contributed equally to this study are now listed as Wenjie Xie and Xin Liu.