Mechanism of Integrin-Mediated Growth Control in Normal, Transformed, and Neoplastic Breast Cells.
Abstract
We are interested in studying the role of integrins in regulating cell proliferation in normal and transformed mammary epithelial cells. During this past year, we found that signals transduced by clustering of integrins were capable of initiating cell proliferation of Go-synchronized normal human mammary epithelial cells (HMEC). Taken together with last year's studies using RGD peptide, it appears that multiple integrins participate in the regulation of cell proliferation of both normal and transformed cells. Surprisingly, fibronectin did not promote the growth of Go-synchronized HMEC while both type I collagen and to a lesser extent laminin-5 had growth promoting effects. This may reflect differences in signaling among the integrins or possibly mechanisms that are active during different stages of the cell cycle. The normal human mammary epithelial cell line MCF-12A and HMEC have similar integrins profiles and similar adhesion capabilities to laminin-5 and fibronectin. However, MCF-12A cells express the breast cancer antigen CA15-3 while HMEC do not. This suggests that MCF-12A cells resemble luminal epithelia while HMEC resemble basal cells. Additional studies are planned to define the signaling pathways utilized by integrins to regulate the proliferation of normal and transformed mammary epithelial cells.
Document Details
- Document Type
- Technical Report
- Publication Date
- Oct 01, 1997
- Accession Number
- ADA337514
Entities
People
- Elizabeth Wayner
- Richard Tamura
Organizations
- Center for Global Infectious Disease Research