Ras-association domain family member 1A (RASSF1A)-where the heart and cancer meet

Trends Cardiovasc Med. 2009 Nov;19(8):262-7. doi: 10.1016/j.tcm.2010.02.008.

Abstract

The close relationship between signaling pathways regulating tumor growth and cardiac hypertrophy has attracted considerable interest. Although the involvement of proto-oncogenes in positively modulating myocardial hypertrophy has long been recognized, little is known about factors that counterregulate them. In this article, we review the novel tumor suppressor Ras-association domain family protein isoform 1A (RASSF1A), which strongly inhibits the prohypertrophic Ras-Raf1-ERK1/2 pathway in the heart. RASSF1A interacts with a number of important signaling molecules regulating cell growth, survival, and apoptosis; therefore, it serves as a key adaptor molecule that integrates the upstream stimuli and transduces them to the selective downstream effectors.

Publication types

  • Review

MeSH terms

  • Animals
  • Cardiomegaly / genetics
  • Cardiomegaly / metabolism*
  • Cardiomegaly / pathology
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Genotype
  • Humans
  • Mice
  • Mice, Knockout
  • Myocardium / metabolism*
  • Myocardium / pathology
  • Neoplasms / genetics
  • Neoplasms / metabolism*
  • Neoplasms / pathology
  • Phenotype
  • Protein Conformation
  • Proto-Oncogene Proteins c-raf / metabolism
  • Signal Transduction* / genetics
  • Structure-Activity Relationship
  • Tumor Suppressor Proteins / chemistry
  • Tumor Suppressor Proteins / deficiency
  • Tumor Suppressor Proteins / genetics
  • Tumor Suppressor Proteins / metabolism*
  • ras Proteins / metabolism

Substances

  • RASSF1 protein, human
  • RASSF1 protein, mouse
  • Tumor Suppressor Proteins
  • Proto-Oncogene Proteins c-raf
  • Extracellular Signal-Regulated MAP Kinases
  • ras Proteins