REST: an oncogene or a tumor suppressor?

Trends Cell Biol. 2013 Jun;23(6):289-95. doi: 10.1016/j.tcb.2013.01.006. Epub 2013 Feb 14.


The Repressor Element-1 (RE-1) Silencing Transcription (REST) factor, which is highly expressed in stem cells and non-neural cells, with low expression in neurons and other neural cells, orchestrates neural differentiation and preserves the unique neural phenotype. REST also plays a role in proliferation, although its effect differs depending on the cell type. It acts as an oncogene in neural cells and tumors (medulloblastomas, neuroblastomas, glioblastomas) and as a tumor suppressor in carcinomas of the lung, breast, and colon. The mechanisms underlying this duality have started to emerge recently and new therapeutic approaches based on these findings are being developed. Here, we present the mechanisms proposed to account for the oncogenic and antioncogenic roles of REST and discuss the therapeutic perspective of recent advances, particularly for small-cell lung cancer.

Publication types

  • Review

MeSH terms

  • Carcinoma / genetics
  • Carcinoma / metabolism
  • Cell Differentiation
  • Cell Proliferation
  • Gene Expression Regulation, Neoplastic
  • Glioblastoma / genetics
  • Glioblastoma / metabolism
  • Humans
  • Medulloblastoma / genetics
  • Medulloblastoma / metabolism
  • Neuroblastoma / genetics
  • Neuroblastoma / metabolism
  • Neurons / metabolism
  • Oncogenes*
  • Repressor Proteins / genetics*
  • Repressor Proteins / metabolism*
  • Stem Cells / metabolism
  • Tumor Suppressor Proteins / genetics*


  • RE1-silencing transcription factor
  • Repressor Proteins
  • Tumor Suppressor Proteins