Cell-Cell Adhesion and Insulin-Like Growth Factor I Receptor in Breast Cancer
Abstract
The structural disintegration of normal epithelium is an early manifestation of cancer in mammary gland. Yet our knowledge on mechanisms controlling breast epithelial cell adhesion is still rudimentary. The increased content of the insulin-like growth factor I receptor (IGF-IR) and its close homologue the insulin receptor (IR) has been well documented in human breast cancer specimens. In this study we investigated how these hormone receptors modulate cell adhesion in breast carcinoma cells. Previously we developed MCF-7 human breast cancer cells overexpressing the IGF-IR. The major achievement of this work is the establishment of a new model consisting of MCF-7-derived cells overexpressing the IR that allowed the comparison of IR and IGF-IR functions. Our results strongly confirmed the specificity of the IGF-IR in promoting the large non-invasive tumor aggregates on biological matrix. For the first time we demonstrated that in breast cancer cells IGF-IR tyrosine kinase modulates the intercellular balance of Beta-catenin, the element of E-cadherin/catenin cell-cell adhesion complex. We continued to explore anti-tumor potentials of the antiestrogens and found that a synthetic steroid analog ICI 182,780 is a potent inhibitor of non-invasive breast tumor aggregates in three-dimensional culture.
Document Details
- Document Type
- Technical Report
- Publication Date
- Sep 01, 1999
- Accession Number
- ADA381131
Entities
People
- Ewa Surmacz
- Marina A. Guvakova
Organizations
- Thomas Jefferson University