The Effects of IGFBP-3 Induction by TGF-B in Breast Tumorigenesis
Abstract
Transforming growth factor Beta (TGF-Beta) is a potent growth inhibitor of normal breast epithelia. Evidence is accumulating that TGF-Beta activity is critical to maintaining the negative paracrine and autocrine regulation of breast epithelial growth. Therefore, defects in the TGF-Beta signaling pathways may result in uncontrolled growth of mammary epithelial cells and consequently contribute to carcinogenesis of the breast. TGF-B acts through a direct mechanism as an inhibitor of proliferation in normal breast epithelium by inducing the expression of the cyclin/ckd inhibitors in several different cell types. Available evidence suggests that TGF-Beta is also able to indirectly mediate its growth inhibitory effects on breast epithelia by inducing the secretion of insulin-like growth factor binding protein 3 (IGFBP-3). IGFBP's are a family of molecules which sequester and prevent insulin-like growth factors (IGF's) from binding and transducing mitogenic signals through the IGF receptors. Our goal is to dissect and elucidate the roles IGF, IGFBP-3, and TGF- Beta in breast tumorigenesis.
Document Details
- Document Type
- Technical Report
- Publication Date
- Sep 01, 1998
- Accession Number
- ADA364148
Entities
People
- Elissa M. Scurry
Organizations
- Duke University