Defects in the regulation of beta-catenin in colorectal cancer

Adv Exp Med Biol. 1999;470:23-32. doi: 10.1007/978-1-4615-4149-3_3.

Abstract

The molecular events that contribute to the progression of colon cancer are beginning to unravel. An initiating and probably obligatory event is the oncogenic activation of beta-catenin. This can come about by the loss of its negative regulator the adenomatous polyposis coli (APC) protein, or by mutations in the beta-catenin gene that result in a more stable protein product. The interaction between APC and beta-catenin, and additional proteins that affect assembly and signaling along this pathway, are discussed.

Publication types

  • Review

MeSH terms

  • Animals
  • Colorectal Neoplasms / genetics
  • Colorectal Neoplasms / metabolism*
  • Cytoskeletal Proteins / biosynthesis
  • Cytoskeletal Proteins / genetics
  • Cytoskeletal Proteins / metabolism*
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Trans-Activators*
  • beta Catenin

Substances

  • CTNNB1 protein, human
  • Cytoskeletal Proteins
  • Trans-Activators
  • beta Catenin