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Objective To explore the biological function and downstream mechanism of ETS1 in glioma. Methods Bioinformatics and immunohistochemistry were used to analyze the differential expression characteristics of ETS1 in gliomas; qRT-PCR was employed to detect the expression level of ETS1 mRNA and lncRNA X-inactive specific transcript (XIST). CCK-8 and 5-ethyl-2′-deoxyuridine experiments were conducted to detect cell growth. Western blot was used to detect the expression of apoptosis-related proteins (Bax, Bak, Bcl-2). PROMO database was utilized to predict the binding sites between ETS1 and XIST promoter. Dual-luciferase reporter gene assay and chromatin immunoprecipitation-quantitative polymerase chain reaction assays were performed to verify the binding relationship between ETS1 and the XIST promoter region. cBioPortal database was used to analyze the correlation between the expression of ETS1 mRNA and XIST in glioma tissues. Results The expression levels of ETS1 mRNA and protein were significantly upregulated in glioma (P

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IntroductionNonalcoholic fatty liver disease (NAFLD) is an epidemic in the obese population. Bariatric surgery is known to reverse multiple metabolic complications of obesity such as diabetes, dyslipidemia, and NAFLD, but the timing of liver changes has not been well described.Materials and methodsThis was an IRB-approved, two-institutional prospective study. Bariatric patients received MRIs at baseline and after a pre-operative liquid diet. Liver biopsies were performed during surgery and if NAFLD positive, the patients received MRIs at 1, 3, and 6 months. Liver volumes and proton-density fat fraction (PDFF) were calculated from offline MRI images. Primary outcomes were changes in weight, body mass index (BMI), percent excess weight loss (EWL%), liver volume, and PDFF. Resolution of steatosis, as defined as PDFF

Objective To explore the effect of long noncoding RNA cancer susceptibility 2 (lncRNA CASC2) on the sensitivity of glioma cells to temazolamide (TMZ) and investigate the underling mechanism. Methods Forty glioma tissue samples derived from the 40 patients undergoing surgical treatment in our department from July 2018 to March 2020 were enrolled in this study. The expression of lncRNA CASC2 in the glioma tissues was detected with RT-PCR, and the results were analyzed with pathological grades and compared between the patients with isocitrate dehydrogenase (IDH) 1/2 mutant (n=17) and IDH 1/2 wild type (n=9). Glioma cells U251 were cultured and transfected with plasmid pc-CASC2 to overexpress lncRNA CASC2 and/or interfering RNA of multi-drug resistance protein ABCG2. CCK-8 assay and flow cytometry were used to detect the cell viability and apoptotic rate in above cell groups after 30 μg/mL TMZ treatment. After mouse intracranial glioma model was established, high performance liquid chromatography was adopted to determine the concentration of TMZ. The correlation between lncRNA CASC2 and ABCG2 was detected by immunofluorescence staining and RNA immunoprecipitation. Results LncRNA CASC2 level was decreased in the glioma tissues with IDH 1/2 wild type, and had a negative correlation with pathological grade of glioma. LncRNA CASC2 overexpression resulted in significantly lower IC50 to TMZ (36.7±4.2 μg/mL) than the U251 cells after pc-Null transfection (t=4.41, P < 0.05). Under 30 μg/mL TMZ stimulation, the cell viability was reduced and the proportion of apoptotic cells was increased after lncRNA-CASC2 overexpression. In the mouse intracranial glioma model, the concentration of intracellular TMZ active product was increased after lncRNA-CASC2 overexpression. LncRNA CASC2 and ABCG2 were evenly distributed in the cytoplasm, and RNA immunoprecipitation showed that the content of lncRNA CASC2 in ABCG2 antibody group was higher than that in IgG control group. In addition, down-regulation of intracellular ABCG2 by siRNA decreased the TMZ sensitivity of U251 cells that could enhanced by lncRNA CASC2. Conclusion LncRNA CASC2 improves the sensitivity of glioma U251 cells to TMZ. However, ABCG2 inhibition by siRNA attenuates the above effects of lncRNA CASC2.

Objective To investigate whether long non-coding (lnc) RNA GASL1 can promote the proliferation of vascular smooth muscle cells (VSMCs) by activating the Wnt/β-catenin signaling pathway. Methods The mRNAs co-expression network related to lncRNA GASL1 was constructed and analyzed with Pathway analysis to predict the signaling pathway of the highest correlation with lncRNA GasL1. After LncRNA GASL1 and lncRNA negative control (lncRNA NC) were transfected into VSMCs respectively, cell counting kit-8 (CCK-8) assay was performed to detect VSMCs viability. Immunofluorescence assay was performed to determine the expression level of proliferation-related protein Bcl-2, and Western blotting to detect the levels of the proteins of Wnt/β-catenin signaling pathway. Finally, Wnt/β-catenin pathway inhibitor ICG001 was added into VSMCs along with lncRNA GASL1 for co-culturing (lncRNA GASL1+ ICG001 group), and the alterations of VSMCs viability and bcl-2 protein level were detected and compared with those in the lncRNA GASL1+ control group. Results There were 374 mRNAs associated with lncRNA GASL1, of which the Wnt/β-catenin pathway had the highest correlation. CCK-8 assay showed that the VSMCs viability was higher in the lncRNA GASL1 group than in the lncRNA NC group (P < 0.05). The results of immunofluorescence assay and Western blotting revealed that both the Bcl-2 protein level and the levels of Wnt1 and β-catenin were increased in lncRNA GASL1 group (P < 0.05) when compared to the lncRNA-NC group. After co-culturing with lncRNA GASL1 and ICG001, the VSMCs viability was significantly decreased (P < 0.05), and the Bcl-2 protein level was decreased when compared with the the lncRNA GASL1+control group (P < 0.05). Conclusion LncRNA GASL1 promotes the proliferation of VSMCs through the Wnt/β-catenin signaling pathway. Blocking the signaling pathway can reduce the promotive effect of lncRNA GASL1 on VSMCs.