Search for Master Regulators in Walking Cancer Pathways

Methods Mol Biol. 2017:1613:161-191. doi: 10.1007/978-1-4939-7027-8_8.

Abstract

In this chapter, we present an approach that allows a causal analysis of multiple "-omics" data with the help of an "upstream analysis" strategy. The goal of this approach is to identify master regulators in gene regulatory networks as potential drug targets for a pathological process. The data analysis strategy includes a state-of-the-art promoter analysis for potential transcription factor (TF)-binding sites using the TRANSFAC® database combined with an analysis of the upstream signal transduction pathways that control the activity of these TFs. When applied to genes that are associated with a switch to a pathological process, the approach identifies potential key molecules (master regulators) that may exert major control over and maintenance of transient stability of the pathological state. We demonstrate this approach on examples of analysis of multi-omics data sets that contain transcriptomics and epigenomics data in cancer. The results of this analysis helped us to better understand the molecular mechanisms of cancer development and cancer drug resistance. Such an approach promises to be very effective for rapid and accurate identification of cancer drug targets with true potential. The upstream analysis approach is implemented as an automatic workflow in the geneXplain platform ( www.genexplain.com ) using the open-source BioUML framework ( www.biouml.org ).

Keywords: ChIP-seq; Microarray data; Pathway analysis; Pathway rewiring; Promoter analysis; RNA-seq; Upstream analysis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents / pharmacology
  • Antineoplastic Agents / therapeutic use
  • Binding Sites
  • Computational Biology / methods*
  • DNA / chemistry
  • DNA / metabolism*
  • Databases, Genetic
  • Gene Expression Regulation, Neoplastic
  • Gene Regulatory Networks / drug effects
  • Humans
  • Molecular Targeted Therapy
  • Neoplasms / drug therapy
  • Neoplasms / genetics*
  • Promoter Regions, Genetic
  • Transcription Factors / metabolism*
  • Web Browser

Substances

  • Antineoplastic Agents
  • Transcription Factors
  • DNA