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Hangzhou, China

Han B.,Hangzhou Dianzi University | Lai H.,Hangzhou Dianzi University | Xie R.,Hangzhou Cancer Institute | Li L.,Hangzhou Dianzi University | Zhu L.,Hangzhou Dianzi University
International Journal of Data Mining and Bioinformatics | Year: 2014

Identifying glioma cancer-alerted genetic markers through analysis of microarray data allows us to detect tumours at the genome-wide level. To this end, we propose to identify glioma gene markers based primarily on their correlation with the glioma diagnostic outcomes, rather than merely on the classifi cation quality or differential expression levels, as it is not the classifi cation or expression level per se that is crucial, but the selection of biologically relevant biomarkers is the most important issue. With the help of singular value decomposition, microarray data are decomposed and the eigenvectors corresponding to the biological effect of diagnostic outcomes are identifi ed. Genes that play important roles in determining this biological effect are thus detected. Therefore, genes are essentially identifi ed in terms of theirstrength of association with diagnostic outcomes. Monte Carlo simulations are then used to fi ne tune the selected gene set in terms of classifi cation accuracy. Experiments show that the proposed method achieves better classifi cation accuracies and is data sets independent. Graph-based statistical analysis showed that the selected genes have close relationships with glioma diagnostic outcomes. Further biological database and literature study confi rms that the identifi ed genes are biologically relevant. © 2014 Inderscience Enterprises Ltd.

Hu Z.,Hangzhou Cancer Institute | Wang W.,Hangzhou Sanatorium of PLA | Ling J.,Hangzhou Sanatorium of PLA | Jiang C.,Hangzhou First Peoples Hospital
Cellular and Molecular Neurobiology | Year: 2016

Microglia-mediated neuroinflammation induced by α-synuclein in the substantianigra likely either initiates or aggravates nigral neuro degeneration in Parkinson’s disease (PD). We aimed to explore the effects of α-mangostin (α-M), a polyphenolicxanthone derivative from mangosteen on α-synuclein-stimulated DA neurodegeneration. Primary microglia, mesencephalic neuron, mesencephalic neuron-glianeuronal cultures, and transwell co-cultures were prepared separately. Liquid scintillation counting was used to determine the radioactivity in DA uptake. Enzyme-linked immunosorbent assay (ELISA) was performed in the IL-1β, IL-6, and TNF-α assay. The expression of proteins was analyzed by Western blot. α-M inhibited the increased levels of pro-inflammatory cytokines, NO, and ROS in α-synuclein-stimulated primary microglia. Mechanistic study revealed that α-M functioned by inhibition of nuclear factor kappa B (NF-κB) and NADPH oxidase. Further, α-M protected α-synuclein-induced microglial and direct neurotoxicity. Although detailed mechanisms remain to be defined, our observations suggest a potential compound, which inhibits microglial activation induced by α-synuclein by targeting NADPH oxidase, might be a therapeutic possibility in preventing PD progression. © 2016 The Author(s)

Hu Z.,Hangzhou Cancer Institute | Wu H.,Hangzhou Cancer Institute | Li Y.,Hangzhou Cancer Institute | Hou Q.,Hangzhou Cancer Institute | And 4 more authors.
Anti-Cancer Drugs | Year: 2014

The study aimed to clarify the relationship between β-elemene, a long noncoding RNA (lncRNA), and human telomerase reverse transcriptase (hTERT) in esophageal carcinoma ECA-109 cells. The proliferation of ECA-109 cells was measured using a CCK-8 kit and flow cytometry. PCR microarray and real-time RT-PCR were designed to determine lncRNA expression in ECA-109 cells before and after treatment with β-elemene. Western blot was used to detect the hTERT level after the differentially expressed lncRNAs in ECA-109 cells were interfered with small interfering RNA (siRNA). On treatment with β-elemene, the proliferation of ECA-109 cells was notably inhibited, and about 85% of the lncRNAs showed higher expression levels in ECA-109 cells than in those untreated cells, from which, CDKN2B-AS1 was screened out. A specific siRNA (si-CDKN2B-AS1) that targets the β-elemene-mediated lncRNA CDKN2B-AS1 was designed, synthesized, and applied to treat ECA-109 cells. Its interference efficiency reached as high as 89.6%. When ECA-109 cells were transfected with the siRNA, the hTERT level was increased by 84.7%. The CCK-8 assay showed that the proliferation of ECA-109 cells treated with β-elemene was significantly promoted after siRNA transfection (P>'0.01). It was also shown by flow cytometry that, compared with the scrambletreated group (negative control), the proliferation index value of ECA-109 cells in the si-CDKN2B-AS1 treatment group was notably increased (25.7 vs. 51.7%) and the TERT protein level was increased by 67.25% after the cells were treated with si-CDKN2B-AS1. The chemotherapeutic drug β-elemene suppressed the proliferation of esophageal carcinoma ECA-109 cells by regulating the inhibition of hTERT expression by lncRNA CDKN2B-AS1. Anti-Cancer Drugs 26:531-539 Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.

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