Abstract

Ovarian cancer (OC) is the highest frequent malignant gynecologic tumor with very complicated pathogenesis. The purpose of the present academic work was to identify significant genes with poor outcome and their underlying mechanisms. Gene expression profiles of GSE36668, GSE14407 and GSE18520 were available from GEO database. There are 69 OC tissues and 26 normal tissues in the three profile datasets. Differentially expressed genes (DEGs) between OC tissues and normal ovarian (OV) tissues were picked out by GEO2R tool and Venn diagram software. Next, we made use of the Database for Annotation, Visualization and Integrated Discovery (DAVID) to analyze Kyoto Encyclopedia of Gene and Genome (KEGG) pathway and gene ontology (GO). Then protein-protein interaction (PPI) of these DEGs was visualized by Cytoscape with Search Tool for the Retrieval of Interacting Genes (STRING). There were total of 216 consistently expressed genes in the three datasets, including 110 up-regulated genes enriched in cell division, sister chromatid cohesion, mitotic nuclear division, regulation of cell cycle, protein localization to kinetochore, cell proliferation and Cell cycle, progesterone-mediated oocyte maturation and p53 signaling pathway, while 106 down-regulated genes enriched in palate development, blood coagulation, positive regulation of transcription from RNA polymerase II promoter, axonogenesis, receptor internalization, negative regulation of transcription from RNA polymerase II promoter and no significant signaling pathways. Of PPI network analyzed by Molecular Complex Detection (MCODE) plug-in, all 33 up-regulated genes were selected. Furthermore, for the analysis of overall survival among those genes, Kaplan–Meier analysis was implemented and 20 of 33 genes had a significantly worse prognosis. For validation in Gene Expression Profiling Interactive Analysis (GEPIA), 15 of 20 genes were discovered highly expressed in OC tissues compared to normal OV tissues. Furthermore, four genes (BUB1B, BUB1, TTK and CCNB1) were found to significantly enrich in the cell cycle pathway via re-analysis of DAVID. In conclusion, we have identified four significant up-regulated DEGs with poor prognosis in OC on the basis of integrated bioinformatical methods, which could be potential therapeutic targets for OC patients.

Highlights

  • Ovarian cancer (OC) is the fifth cause of cancerous death among women all over the world [1]

  • Results showed that a total of 216 commonly Differentially expressed genes (DEGs) were detected, including 106 downregulated genes and 110 up-regulated genes in the OC tissues (Table 1 & Fig. 1)

  • DEGs gene ontology and Kyoto Encyclopedia of Gene and Genome (KEGG) pathway analysis in ovarian cancers All 216 DEGs were analyzed by DAVID software and the results of GO analysis indicated that 1) for biological processes (BP), up-regulated DEGs were enriched in regulation of cell cycle, cell division, mitotic nuclear division, protein localization to kinetochore, Table 1 All 216 commonly differentially expressed genes (DEGs) were detected from three profile datasets, including 106 downregulated genes and 110 up-regulated genes in the OC tissues compared to normal OV tissues

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Summary

Introduction

Ovarian cancer (OC) is the fifth cause of cancerous death among women all over the world [1]. Some prognostic biomarkers have been exploited, the overall survival of OC remains weak due to its difficulty in early detection, distant metastasis and rapid dissemination [2, 3]. More reliable prognostic biomarkers should be explored as a target for improving the treatment effect and better understanding the underlying mechanism. Gene chip which was used for more than ten years can quickly detect differentially expressed genes and was proved to be a reliable technique [4] that could make many slice data be produced and stored in public databases. A large number of valuable clues could be explored for new research on the base of these data. Many bioinformatical studies on OC have been produced in recent years [5], which proved that the

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