Regulation of the insulin-like growth factor-I receptor gene by oncogenes and antioncogenes: Implications in human cancer

Haim Werner*, Michal Shalita-Chesner, Shirley Abramovitch, Gila Idelman, Limor Shaharabani-Gargir, Tova Glaser

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

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 acclivity. 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. (C) 2000 Academic Press.

Original languageEnglish
Pages (from-to)315-320
Number of pages6
JournalMolecular Genetics and Metabolism
Volume71
Issue number1-2
DOIs
StatePublished - 2000

Funding

FundersFunder number
John E. Fogarty International Center
Ministry of Health of Israel
Rashi Foundation, Israel
Recanati Foundation
U.S.–Israel Binational Science Foundation
National Institutes of Health
Israel Cancer Research Fund
Israel Academy of Sciences and Humanities
Israel Cancer Association

    Keywords

    • BRCA1
    • Gene expression
    • IGF-I receptor
    • Oncogenes
    • Transcription
    • Tumor suppressor
    • WT1
    • p53

    Fingerprint

    Dive into the research topics of 'Regulation of the insulin-like growth factor-I receptor gene by oncogenes and antioncogenes: Implications in human cancer'. Together they form a unique fingerprint.

    Cite this