TY - JOUR
T1 - Regulation of the insulin-like growth factor-I receptor gene by oncogenes and antioncogenes
T2 - Implications in human cancer
AU - Werner, Haim
AU - Shalita-Chesner, Michal
AU - Abramovitch, Shirley
AU - Idelman, Gila
AU - Shaharabani-Gargir, Limor
AU - Glaser, Tova
N1 - Funding Information:
The work in the authors’ laboratory is supported by grants from The Israel Cancer Association, The Ministry of Health of Israel, The Israel Academy of Sciences, The U.S.–Israel Binational Science Foundation, The Israel Cancer Research Fund (New York), The Recanati Foundation (Tel Aviv), and The John E. Fogarty International Center (NIH, U.S.). H.W. is the recipient of a Guastalla Fellowship, The Rashi Foundation, Israel.
PY - 2000
Y1 - 2000
N2 - 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.
AB - 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.
KW - BRCA1
KW - Gene expression
KW - IGF-I receptor
KW - Oncogenes
KW - Transcription
KW - Tumor suppressor
KW - WT1
KW - p53
UR - http://www.scopus.com/inward/record.url?scp=0033808766&partnerID=8YFLogxK
U2 - 10.1006/mgme.2000.3044
DO - 10.1006/mgme.2000.3044
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AN - SCOPUS:0033808766
SN - 1096-7192
VL - 71
SP - 315
EP - 320
JO - Molecular Genetics and Metabolism
JF - Molecular Genetics and Metabolism
IS - 1-2
ER -
