RAS/ERK pathway transcriptional regulation through ETS/AP-1 binding sites

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

The RAS/RAF/MEK/ERK signaling pathway is activated by mutation in many cancers. Neighboring ETS and AP-1 DNA binding sequences can act as response elements for transcriptional activation by this pathway. ERK phosphorylation of an ETS transcription factor is one mechanism of activating the RAS/ERK gene expression program that can promote cancer cell phenotypes such as proliferation, invasion and metastasis. Recent genome-wide mapping of ETS proteins overexpressed by chromosomal rearrangement in prostate cancer reveals a second mechanism for activation of this gene expression program. An oncogenic subset of ETS transcription factors can activate RAS/ERK target genes even in the absence of RAS/ERK pathway activation by binding ETS/AP-1 sequences. Thus, regulation of cancer cell invasion and metastasis via ETS/AP-1 sequence elements depends on which ETS protein is bound, and the status of the RAS/ERK pathway. This commentary will focus on what is known about the selectivity of ETS/AP-1 sequences for different ETS transcription factors and the transcriptional consequences of ETS protein selection.

Original languageEnglish
Pages (from-to)1-5
Number of pages5
JournalSmall GTPases
Volume3
Issue number3
StatePublished - 2012

Fingerprint

MAP Kinase Signaling System
Transcription Factor AP-1
Binding Sites
Transcription Factors
Chemical activation
Gene expression
Genes
Cells
Neoplasm Metastasis
Gene Expression
Neoplasms
Phosphorylation
Proteins
Chromosome Mapping
Mitogen-Activated Protein Kinase Kinases
Response Elements
Transcriptional Activation
Prostatic Neoplasms
Phenotype
Mutation

Keywords

  • AP-1
  • Cell migration
  • ERK
  • ETS
  • Prostate cancer
  • RAS signaling
  • Transcription

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology

Cite this

RAS/ERK pathway transcriptional regulation through ETS/AP-1 binding sites. / Hollenhorst, Peter.

In: Small GTPases, Vol. 3, No. 3, 2012, p. 1-5.

Research output: Contribution to journalArticle

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