Aberrant receptor signaling and trafficking as mechanisms in oncogenesis

Crit Rev Oncog. 2007 Aug;13(1):39-74. doi: 10.1615/critrevoncog.v13.i1.20.

Abstract

Intracellular signaling pathways activated through cell surface receptors are essential for cell proliferation, differentiation, survival, and migration. Dysregulation of such signaling through mutations, chromosome rearrangements, aberrant gene expression, or epigenetic changes is a key factor in oncogenesis. Prominent examples of receptor signaling pathways that are dysregulated in cancers include those initiated by receptor tyrosine kinases, WNT, TGFbeta, and Notch receptors. In this review we will discuss these signaling pathways and how their dysfunction may contribute to oncogenesis. We will also highlight the important role of endocytic membrane trafficking in receptor signaling and tumor suppression.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Cell Transformation, Neoplastic*
  • Endocytosis
  • Humans
  • Protein Transport*
  • Receptor Protein-Tyrosine Kinases / metabolism*
  • Signal Transduction*

Substances

  • Receptor Protein-Tyrosine Kinases