Is β-Catenin a Druggable Target for Cancer Therapy?

Trends Biochem Sci. 2018 Aug;43(8):623-634. doi: 10.1016/j.tibs.2018.06.003. Epub 2018 Jul 2.

Abstract

Mutations of canonical Wnt signaling pathway genes frequently occur in cancer and lead to abnormal accumulation of the key effector β-catenin. Over the past decades, a number of Wnt inhibitors have been identified through high-throughput screenings, however, very few of them target β-catenin directly, raising questions regarding its druggability. Here, we review Wnt inhibitors with a focus on small molecules that directly bind β-catenin, discuss the druggability of β-catenin, and why it has rarely been targeted, especially in the cellular context. We also propose strategies to develop small molecule binding and depleting cellular β-catenin, which are generally applicable to other difficult-to-drug or yet-to-be-drugged targets.

Keywords: cancer; druggability; interaction in vivo; intrinsically disordered protein region; protein depletion; β-catenin.

Publication types

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

MeSH terms

  • Antineoplastic Agents / pharmacology
  • Antineoplastic Agents / therapeutic use
  • Humans
  • Intrinsically Disordered Proteins / metabolism
  • Neoplasms / drug therapy*
  • Neoplasms / metabolism
  • Wnt Signaling Pathway / drug effects
  • beta Catenin / drug effects*
  • beta Catenin / metabolism

Substances

  • Antineoplastic Agents
  • CTNNB1 protein, human
  • Intrinsically Disordered Proteins
  • beta Catenin