BackgroundCancers are caused by the acquisition of somatic mutations. Numerous efforts have been made to characterize the key driver genes and pathways in glioma, however, the etiology of glioma is still not completely known. This study was implemented to characterize driver genes in glioma independently of somatic mutation frequencies.MethodsDriver genes and pathways were predicted by OncodriveCLUST, OncodriveFM, Icages, Drgap and Dendrix in glioma using 31,958 somatic mutations from TCGA, followed by an integrative characterization of driver genes.ResultsOverall, 685 driver genes and 215 driver pathways were determined by the five tools. FSTL5, HCN1, TMEM132D, TRHDE and KRT222 showed the strongest expression correlation with other genes in the co-expression network of glioma tissues. ST6GAL2, PIK3CA, PIK3R1, TP53 and EGFR are at the core of the protein–protein interaction network. 133 driver genes were up-regulated and associated to poor prognosis, 43 driver genes were down-regulated and related to favorable clinical outcome in glioma patients. The driver genes such as MSH6 and RUNX1T1 might serve as candidate prognostic biomarkers and therapeutic targets in glioma.ConclusionsThe set of new cancer genes and pathways sheds insights into the tumorigenesis of glioma and paves the way for developing driver gene-targeted therapy and prognostic biomarkers in glioma.Electronic supplementary materialThe online version of this article (doi:10.1186/s12935-017-0458-y) contains supplementary material, which is available to authorized users.

BackgroundTo investigate antioxidant effects of traditional Chinese Shengjing capsule extracts (sperm-producing capsule, with functions of tonifying kidney and invigorating kidney essence) on testes, epididymides, and sperms of rats.Material/MethodsWe randomly divided 50 rats into 5 groups. G1: normal control group (treated with saline); G2: cadmium chloride group; G3: cadmium chloride+ low doses of drugs; G4: cadmium chloride + medium doses of drugs; and G5: cadmium chloride + high doses of drugs (equivalent dose: 0.45 g/kg). In addition to the normal control group, the other 4 groups started receiving intraperitoneal injection of cadmium chloride (1 mg/kg, i.p.). Testicular glutathione peroxidase (GSH-PX), superoxide dismutase (SOD), and malondialdehyde aldehyde (MDA) were measured by ELISA; epididymis histopathological examination was performed; testis serum testosterone (T) was measured; specimens of the epididymal semen were analyzed for sperm concentration, morphology, vitality, and DNA fragmentation rate.ResultsSperm count and activity of rats in the model control group decreased significantly; their MDA concentration of testicular and epididymal homogenates increased greatly; while the vitality of SOD and GSH-Px dropped sharply. All indexes mentioned above were significantly different from those of the blank control group (P<0.05); the sperm count and activity of rats treated with Shengjing capsule (sperm-producing capsule) decreased, but were still significantly higher than those of the model group (P<0.05). MDA level of rats treated with Shengjing capsule were significantly lower than that of the model group (P<0.05), while their SOD and GSH-Px activity were significantly higher than the model group (P<0.05). The normal morphology rate and DNA integrity rate of groups treated with Shengjing capsule were significantly higher than those of the model group (P<0.05).ConclusionsShengjing can enhance the activity of antioxidant enzymes and inhibit oxidative stress. It can also repair testicular and epididymal pathological damages, protect spermatogenesis, increase sperm count and activity, and improve normal morphology rate of sperm.

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Background: PYD and CARD domain-containing (PYCARD) was upregulated in TMZ-resistant cell lines and glioma tissue and was correlated with poor prognosis, its role in glioma is unclear known. The aim of this study was to elucidate the relationship between PYCARD and glioma based on Gene Expression Omnibus (GEO), The Cancer Genome Atlas (TCGA), and Chinese Glioma Genome Atlas (CGGA) databases.Methods: Glioma-resistant cells were compared with parental cells based on the GSE53014 and GSE113510 data sets. The relationship between PYCARD, tumor microenvironment, and long noncoding RNAs (lncRNAs) was assessed using logistic regression. Moreover, Kaplan-Meier and Cox regression were used to analyze the relationship between PYCARD expression and survival rate. Gene set enrichment analysis (GSEA) was also used to determine the biological function of PYCARD and lncRNAs. Cell viability and cell migration assays were used to evaluate the ability of cells to migrate and proliferate. Finally, we analyzed the expression patterns of PYCARD genes in a wide range of cancers.Results: Elevated expression of PYCARD promoted glioma cell proliferation and migration. PYCARD expression was significantly positively associated with gamma delta T cells but negatively correlated with M2 macrophages in glioblastoma multiforme (GBM). Likewise, PYCARD expression was significantly positively associated with monocytes but negatively associated with activated mast cells in low grade glioma (LGG).We also found that 3 PYCARD-related lncRNAs in GBM and 4 PYCARD-related lncRNAs in LGG had a predictive value for glioma patients. The pan-cancer analysis showed that PYCARD expression was higher in most cancer groups.Conclusions: High expression of PYCARD is an independent predictor of unfavorable prognosis and chemotherapy resistance in glioma.