Mechanisms by which Distinct ErbB Receptor Homo- and Heterodimers Reinitiate Proliferation in Growth-Arrested, Polarized, Epithelial Structures

Abstract

Using three-dimensional epithelial culture and inducible Erb3 activation methods, we analyzed the ability of ErbB2/ErbB3 heterodimer to induce proliferation of epithelial cells in acini, and investigated the mechanism by which ErbB2 regulates cell cycle progression. Our data shown that ErbB2/ErbB3 heterodimer has stronger ability to initiate proliferation of growth-arrested cell in acini, meanwhile, to protect cells from apoptosis, compared to ErbB2 homodimer. Cyclin D1, D3 and E1 are required for normal morphogenesis of 3D acini, but only cyclin E1 is required for ErbB2-induced proliferation. ErbB2-overexpressed breast cancer cell lines or primary tumors have higher levels of cyclin E.

Open PDF

Document Details

Document Type
Technical Report
Publication Date
Jun 01, 2004
Accession Number
ADA430630

Entities

People

  • Bin Xiang

Organizations

  • Cold Spring Harbor Laboratory

Tags

DTIC Thesaurus Topics

  • Abstracts
  • Antigens
  • Apoptosis
  • Breast Cancer
  • Cell Line
  • Cell Physiological Processes
  • Cells
  • Culture Techniques
  • Epithelial Cells
  • Growth Factors
  • Mammary Glands
  • Morphogenesis
  • Neoplasms
  • Three Dimensional

Readers

  • Breast cancer cell signaling and growth regulation.
  • Molecular and Cellular Biochemistry