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Article
β-Catenin and Tcfs in Mammary Development and Cancer
Journal of Mammary Gland Biology and Neoplasia (2003)
  • Sarah Hatsell
  • Tracey Rowlands
  • Minoti Hiremath
  • Pamela Cowin
Abstract

β-Catenin regulates cell–cell adhesion and transduces signals from many pathways to regulate the transcriptional activities of Tcf/Lef DNA binding factors. Gene ablation and transgenic expression studies strongly support the concept that β-catenin together with Lef/Tcf factors act as a switch to determine cell fate and promote cell survival and proliferation at several stages during mammary gland development. Mice expressing the negative regulator of Wnt/β-catenin signaling (K14-Dkk) fail to form mammary buds, and those lacking Lef-1 show an early arrest in this process at stage E13.5. Stabilized N89 β-catenin initiates precocious alveologenesis during pubertal development, and negative regulators of endogenous β-catenin signaling suppress normal alveologenesis during pregnancy. Stabilized β-catenin induces hyperplasia and mammary tumors in mice. Each of the β-catenin-induced phenotypes is accompanied by upregulation of the target genes cyclin D1 and c-myc. Cyclin D1, however, is dispensable for tumor formation and the initiation of alveologenesis but is essential for later alveolar expansion.

Keywords
  • catenin,
  • Lef,
  • Tcf,
  • cyclins,
  • MUC,
  • Wnt
Publication Date
April, 2003
Citation Information
Sarah Hatsell, Tracey Rowlands, Minoti Hiremath and Pamela Cowin. "β-Catenin and Tcfs in Mammary Development and Cancer" Journal of Mammary Gland Biology and Neoplasia Vol. 8 Iss. 2 (2003)
Available at: http://works.bepress.com/minoti_hiremath/6/