GC patients with an elevated CTGF expression have more lymph node metastases and a shorter survival time. CTGF seems to be an independent prognostic factor for the successful differentiation of high-risk GC patients staging I + II + III. Over-expression of CTGF in human GC cells results in an increased aggressive ability.

BackgroundRubber tree (Hevea brasiliensis Muell. Arg.) is the primarily commercial source of natural rubber in the world. Latex regeneration and duration of latex flow after tapping are the two factors that determine rubber yield of rubber tree, and exhibit a huge variation between rubber tree clones CATAS8-79 and PR107.ResultsTo dissect the molecular mechanism for the regulation of latex regeneration and duration of latex flow, we sequenced and comparatively analyzed latex of rubber tree clone CATAS8-79 and PR107 at transriptome level. More than 26 million clean reads were generated in each pool and 51,829 all-unigenes were totally assembled. A total of 6,726 unigenes with differential expression patterns were detected between CATAS8-79 and PR107. Functional analysis showed that genes related to mass of categories were differentially enriched between the two clones. Expression pattern of genes which were involved in latex regeneration and duration of latex flow upon successive tapping was analyzed by quantitative PCR. Several genes related to rubber biosynthesis, cellulose and lignin biosynthesis and rubber particle aggregation were differentially expressed between CATAS8-79 and PR107.ConclusionsThis is the first report about probing latex regeneration and duration of latex flow by comparative transcriptome analysis. Among all the suggested factors, it is more important that the level of endogenous jasmonates, carbohydrate metabolism, hydroxymethylglutaryl-CoA reductase (HMGR) and Hevea rubber transferase (HRT) in mevalonate (MVA) parthway for latex regeneration while the level of endogenous ethylene (ETH), lignin content of laticifer cell wall, antioxidants and glucanases for the duration of latex flow. These data will provide new cues for understanding the molecular mechanism for the regulation of latex regeneration and duration of latex flow in rubber tree.Electronic supplementary materialThe online version of this article (doi:10.1186/s12870-015-0488-3) contains supplementary material, which is available to authorized users.

Two contrasting cold response rubber tree clones, the cold-resistant ‘93-114’ and cold-sensitive ‘Reken501’, were subject to a global transcriptome response assessing via high-throughput RNA-seq technique and comprehensive bioinformatics analysis using the referenced rubber tree genome with the purpose of exploring the potential molecular cues underlying the tolerance of rubber trees to cold stress. As a result, a total of 1919 genes had significantly higher expression, while 2929 genes had significantly lower expression in ‘93–114’ than in ‘Reken501’ without cold stress. Upon cold stress, the numbers of genes with significantly higher expression decreased to 1501 at 1 h treatment and to 1285 at 24 h treatment in ‘93–114’ than that of ‘Reken501’, conversely, the numbers of genes with significantly lower expression increased to 7567 at 1 h treatment and to 5482 at 24 h treatment. Functional annotation of the differentially expressed genes between ‘93–114’ and ‘Reken501’ suggests that down-regulation of auxin and ethylene signaling and activation of heat shock module and ROS scavengers is a primary strategy for H. brasiliensis to cope with cold stress. Our identified vital differentially expressed genes may be beneficial for elucidation of the molecular mechanisms underlying cold tolerance and for genetic improvement of H. brasiliensis clones.

Epithelial ovarian cancer (EOC) is one of the malignancies in women, which has the highest mortality. However, the microlevel mechanism has not been discussed in detail. The expression profiles GSE27651, GSE38666, GSE40595, and GSE66957 including 188 tumor and 52 nontumor samples were downloaded from the Gene Expression Omnibus database. The differentially expressed genes (DEGs) were filtered using R software, and we performed functional analysis using the clusterProfiler. Cytoscape software, the molecular complex detection plugin and database STRING analyzed DEGs to construct protein-protein interaction network. We identified 116 DEGs including 81 upregulated and 35 downregulated DEGs. Functional analysis revealed that they were significantly enriched in the extracellular region and biosynthesis of amino acids. We next identified four bioactive compounds (vorinostat, LY-294002,trichostatin A, and tanespimycin) based on ConnectivityMap. Then 114 nodes were obtained in protein–protein interaction. The three most relevant modules were detected. In addition, according to degree ≥ 10, 14 core genes including FOXM1, CXCR4, KPNA2, NANOG, UBE2C, KIF11, ZWINT, CDCA5, DLGAP5, KIF15, MCM2, MELK, SPP1, and TRIP13 were identified. Kaplan–Meier analysis, Oncomine, and Gene Expression Profiling Interactive Analysis showed that overexpression of FOXM1, SPP1, UBE2C, KIF11, ZWINT, CDCA5, UBE2C, and KIF15 was related to bad prognosis of EOC patients. CDCA5, FOXM1, KIF15, MCM2, and ZWINT were associated with stage. Receiver operating characteristic (ROC) curve showed that messenger RNA levels of these five genes exhibited better diagnostic efficiency for normal and tumor tissues. The Human Protein Atlas database was performed. The protein levels of these five genes were significantly higher in tumor tissues compared with normal tissues. Functional enrichment analysis suggested that all the hub genes played crucial roles in citrate cycle tricarboxylic acid cycle. Furthermore, the univariate and multivariate Cox proportional hazards regression showed that ZWINT was independent prognostic indictor among EOC patients. The genes and pathways discovered in the above studies may open a new direction for EOC treatment.

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Background: Endometrial cancer (EC) is one kind of women cancers. Bioinformatic technology could screen out relative genes which made targeted therapy becoming conventionalized. Methods: GSE17025 were downloaded from GEO. The genomic data and clinical data were obtained from TCGA. R software and bioconductor packages were used to identify the DEGs. Clusterprofiler was used for functional analysis. STRING was used to assess PPI information and plug-in MCODE to screen hub modules in Cytoscape. The selected genes were coped with functional analysis. CMap could find EC-related drugs that might have potential effect. Univariate and multivariate Cox proportional hazards regression analyses were performed to predict the risk of each patient. Kaplan-Meier curve analysis could compare the survival time. ROC curve analysis was performed to predict value of the genes. Mutation and survival analysis in TCGA database and UALCAN validation were completed. Immunohistochemistry staining from Human Protein Atlas database. GSEA, ROC curve analysis, Oncomine and qRT-PCR were also performed. Results: Functional analysis showed that the upregulated DEGs were strikingly enriched in chemokine activity, and the down-regulated DEGs in glycosaminoglycan binding. PPI network suggested that NCAPG was the most relevant protein. CMap identified 10 small molecules as possible drugs to treat EC. Cox analysis showed that BCHE, MAL and ASPM were correlated with EC prognosis. TCGA dataset analysis showed significantly mutated BHCE positively related to EC prognosis. MAL and ASPM were further validated in UALCAN. All the results demonstrated that the two genes might promote EC progression. The profile of ASPM was confirmed by the results from immunohistochemistry. ROC curve demonstrated that the mRNA levels of two genes exhibited difference between normal and tumor tissues, indicating their diagnostic efficiency. qRT-PCR results supported the above results. Oncomine results showed that DNA copy number variation of MAL was significantly higher in different EC subtypes than in healthy tissues. GSEA suggested that the two genes played crucial roles in cell cycle. Conclusion: BCHE, MAL and ASPM are tumor-related genes and can be used as potential biomarkers in EC treatment.

Circulating tumor cells (CTCs) have attracted pretty much attention from scientists because of their important relationship with the process of metastasis. Here, we developed a size-based microfluidic chip containing triangular pillar array and filter channel array for detecting single CTCs and CTC clusters independent of tumor-specific markers. The cell populations in chip were characterized by immune-fluorescent staining combining an epithelial marker and a mesenchymal marker. We largely decreased the whole time of detection process to nearly 1.5h with this microfluidic device. The CTCs were subsequently measured in 77 patients with lung cancer and 39 healthy persons. The microfluidic device allowed for the detection of CTCs with apparent high sensitivity and specificity (82.7% sensitivity and 100% specificity). Furthermore, the total CTC counts were found to be elevated in advanced patients with metastases when compared with those without (20.89±14.57 vs 8.428±5.858 cells/mL blood; P<0.01). Combined epithelial marker and mesenchymal marker analysis of CTCs could provide more information about metastasis in patients than only usage of epithelial marker. In conclusion, the development of the size-based microfluidic device for efficient capture of CTCs will enable detailed characterization of their biological properties and values in cancer diagnosis.