Copy number loss or silencing of apoptosis-effector genes in cancer

Gene. 2015 Jan 1;554(1):50-7. doi: 10.1016/j.gene.2014.10.021. Epub 2014 Oct 11.

Abstract

Cancer cells undergo a variety of DNA copy number gains and losses (CNV), raising two important questions related to cancer development: (i) Which genes are affected? (ii) And how do CNVs, that do not represent complete deletions but do represent gene-dosage alterations, impact cancer cell functions? Recent studies have indicated that CNVs in cancer can impact genes for regulatory proteins long known to be associated with cancer development, but less is understood about CNVs affecting effector genes. Also, we have recently indicated the likely importance of transcription factor binding site (TFBS) copies in effector genes, in regulating the transition from a proliferative to an apoptotic state. Here we report data-mining analyses that indicate that copies of apoptosis-effector genes are commonly lost in cancer development, in comparison to proliferation-effector genes, and when not, apoptosis effector genes have silenced chromatin structures.

Keywords: Apoptosis-effector genes; COSMIC; Copy number variation; ENCODE; Gene dosage; TCGA.

MeSH terms

  • Apoptosis*
  • Cell Proliferation
  • Chromatin / metabolism
  • Computational Biology
  • DNA Copy Number Variations*
  • Data Mining
  • Gene Dosage*
  • Gene Expression Regulation, Neoplastic*
  • Gene Silencing*
  • Genome, Human
  • Humans
  • Mutation
  • Neoplasms / genetics*
  • Transcription Factors / metabolism
  • Tumor Suppressor Protein p53 / metabolism

Substances

  • Chromatin
  • TP53 protein, human
  • Transcription Factors
  • Tumor Suppressor Protein p53