학술논문
Regulation of the Insulin-Like Growth Factor-I Receptor Gene by Oncogenes and Antioncogenes: Implications in Human Cancer
Document Type
Article
Author
Source
Molecular Genetics and Metabolism; September 2000, Vol. 71 Issue: 1-2 p315-320, 6p
Subject
Language
ISSN
10967192; 10967206
Abstract
The insulin-like growth factor-I receptor (IGF-I-R) has a central role in normal cellular proliferation as well as in transformation processes. Transcription of the IGF-I receptor gene is controlled by a number of tumor suppressors, including WT1, p53, and BRCA1. It has been demonstrated that, in their wild-type form, these transcription factors can suppress the activity of the IGF-I-R promoter, with ensuing reduction in the levels of cell-surface IGF binding. On the other hand, a number of oncogenes, including mutant p53 and c-myb, and the fusion protein EWS-WT1 significantly stimulate promoter activity. Interactions between stimulatory and inhibitory transcription factors may determine the level of expression of the IGF-I-R gene and, consequently, the proliferative status of the cell.