Differentially Expressed Genes and Signature Pathways of Human Prostate Cancer

PLoS One. 2015 Dec 18;10(12):e0145322. doi: 10.1371/journal.pone.0145322. eCollection 2015.

Abstract

Genomic technologies including microarrays and next-generation sequencing have enabled the generation of molecular signatures of prostate cancer. Lists of differentially expressed genes between malignant and non-malignant states are thought to be fertile sources of putative prostate cancer biomarkers. However such lists of differentially expressed genes can be highly variable for multiple reasons. As such, looking at differential expression in the context of gene sets and pathways has been more robust. Using next-generation genome sequencing data from The Cancer Genome Atlas, differential gene expression between age- and stage- matched human prostate tumors and non-malignant samples was assessed and used to craft a pathway signature of prostate cancer. Up- and down-regulated genes were assigned to pathways composed of curated groups of related genes from multiple databases. The significance of these pathways was then evaluated according to the number of differentially expressed genes found in the pathway and their position within the pathway using Gene Set Enrichment Analysis and Signaling Pathway Impact Analysis. The "transforming growth factor-beta signaling" and "Ran regulation of mitotic spindle formation" pathways were strongly associated with prostate cancer. Several other significant pathways confirm reported findings from microarray data that suggest actin cytoskeleton regulation, cell cycle, mitogen-activated protein kinase signaling, and calcium signaling are also altered in prostate cancer. Thus we have demonstrated feasibility of pathway analysis and identified an underexplored area (Ran) for investigation in prostate cancer pathogenesis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Gene Expression Profiling
  • Gene Expression Regulation, Neoplastic
  • Gene Ontology
  • Humans
  • Male
  • Middle Aged
  • Prostatic Neoplasms / genetics
  • Prostatic Neoplasms / metabolism*
  • Signal Transduction
  • TGF-beta Superfamily Proteins / genetics
  • TGF-beta Superfamily Proteins / metabolism
  • Transcriptome

Substances

  • TGF-beta Superfamily Proteins

Grants and funding

This work was in part supported by the Leslie N. Wilson-Delores Auzenne Graduate Assistantship for Minorities awarded to JSM by the Florida State University Graduate School, the Research Experience Program of Women in Math, Science, and Engineering of Florida State University to AKVL, and grants from the Florida State University and an Endowed Chair Professorship in Cancer Research from anonymous donors to QXAS. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.