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• Research Paper Volume 12, Issue 1 pp 178-192

  Genome-wide DNA copy number profiling and bioinformatics analysis of ovarian cancer reveals key genes and pathways associated with distinct invasive/migratory capabilities

  Relevance score: 24.769978

  GuiFen Liu, GuanYu Ruan, MeiMei Huang, LiLi Chen, PengMing Sun

  Keywords: copy number variations (CNVs), protein/DNA array, ovarian cancer, invasion, metastasis

  Published in Aging on January 2, 2020

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  Ovarian cancer (OC) metastasis presents major hurdles that must be overcome to improve patient outcomes. Recent studies have demonstrated copy number variations (CNVs) frequently contribute to alterations in oncogenic drivers. The present study used a CytoScan HD Array to analyse CNVs and loss of heterozygosity (LOH) in the entire genomes of 6 OC patients and human OC cell lines to determine the genetic target events leading to the distinct invasive/migratory capacities of OC. The results showed that LOH at Xq11.1 and Xp21.1 and gains at 8q21.13 were novel, specific CNVs. Ovarian cancer-related CNVs were then screened by bioinformatics analysis. In addition, transcription factors-target gene interactions were predicted with information from PASTAA analysis. As a result, six genes (i.e., GAB2, AKT1, EGFR, COL6A3, UGT1A1 and UGT1A8) were identified as strong candidates by integrating the above data with gene expression and clinical outcome data. In the transcriptional regulatory network, 4 known cancer-related transcription factors (TFs) interacted with 6 CNV-driven genes. The protein/DNA arrays revealed 3 of these 4 TFs as potential candidate gene-related transcription factors in OC. We then demonstrated that these six genes can serve as potential biomarkers for OC. Further studies are required to elucidate the pathogenesis of OC.

  

  Illustration of the copy number state of all samples. Chromosomes 1 through 12 are shown in the upper panel (from left to right), chromosomes 13 through 22 are shown in the lower panel, and chromosomes X and Y are shown in the lower right panel. Six samples were included (LXM, WXL, YLH, and ZLQ: OC; and GRY and NDY: normal epithelial OC). Colour indicates copy number status (blue, duplication; red, deletion; purple, LOH); greater colour saturation indicates greater CNV.

  
  
  

  

  Different biological behaviours and CNVs in OC cell lines. The migration distance in the HO-8910 cell line was less than that in the HO-8910PM cell line (p <0.01) (A). Cells were incubated on migration wells for 48 h, and the number of cells that migrated to the lower side of the filter was counted (B). The results are shown as the mean ± standard deviation (SD) (p <0.01 compared to the HO-8910 cell line). (C) Circos plot of the segmented CNVs in HO-8910PM (inner race) and HO-8910 (outer race) cell lines. Coloured bands expanding towards the centre or periphery of the diagram represent copy number losses or gains, respectively (red, gain; blue, loss).

  
  
  

  

  Functional enrichment analysis of “HO-8910PM-specific gain” and “HO-8910PM-specific loss” genes identified in CNV regions. (A) GO-based annotation was used for the functional enrichment analysis of genes with shared “HO-8910PM-specific gains” (479 genes). (B) KEGG pathway analysis of genes with shared “HO-8910PM-specific gains” (479 genes). (C) GO-based annotation was used for the functional enrichment analysis of genes with shared “HO-8910PM-specific loss” (400 genes) through DAVID. (D) KEGG pathway analysis of genes with shared “HO-8910PM-specific loss” (400 genes). Colour represents the -log of the P value for the significance of enrichment. Only annotations with significant P values < 0.05 are shown.

  
  
  

  

  PPI network based on 71 genes. There are 54 nodes and 112 edges in the network. Nodes represent genes, and edges represent the interactions between genes.

  
  
  

  

  The expression of six genes predicts the prognosis of OC patients. The prognostic values of the six genes in OC patients were determined (P < 0.05).

  
  
  

  

  The target genes and their predicted TFs. (A) The clusters identified in the PPI network containing the target genes and their predicted TFs. (B) The transcriptional activities of four TFs.