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J. Biol. Chem., Vol. 276, Issue 21, 18185-18192, May 25, 2001
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From the The activated insulin-like growth factor-I
receptor (IGF-IR) is implicated in mitogenesis, transformation, and
anti-apoptosis. To investigate the role of the IGF-IR in protection
from UV-mimetic-induced DNA damage, 4-nitroquinoline
N-oxide (4-NQO) was used. In this study we show that the
activation of the IGF-IR is capable of rescuing NWTb3 cells
overexpressing normal IGF-IRs from 4-NQO-induced DNA damage as
demonstrated by cellular proliferation assays. This action was specific
for the IGF-IR since cells expressing dominant negative IGF-IRs were
not rescued from 4-NQO UV-mimetic treatment. DNA damage induced by
4-NQO in NWTb3 cells was significantly decreased after IGF-IR
activation as measured by comet assay. IGF-I was also able to overcome
the cell cycle arrest, observed after 4-NQO treatment, thereby
enhancing the ability of NWTb3 cells to enter S phase. Interestingly,
the p38 mitogen-activated protein kinase pathway was shown to represent
the main signaling pathway involved in the IGF-IR-mediated rescue of
UV-like damaged cells. The ability of the IGF-IR to induce DNA repair
was also demonstrated by infecting NWTb3 cells with UV-irradiated
adenovirus. Activation of the IGF-IR resulted in enhanced
Insulin-like Growth Factor-I (IGF-I) Receptor Activation
Rescues UV-damaged Cells through a p38 Signaling Pathway
POTENTIAL ROLE OF THE IGF-I RECEPTOR IN DNA REPAIR*
,,¶
Section on Cellular and Molecular
Physiology, Clinical Endocrinology Branch, NIDDK and § Gene
Therapy and Therapeutics Branch, NIDCR, National Institutes of
Health, Bethesda, Maryland 20892-1758
-galactosidase reporter gene activity demonstrating repair of the
damaged DNA. This study indicates a direct role of the IGF system in
the rescue of damaged cells via DNA repair.
*
This study was supported by a Fondation pour la Recherche
Médicale grant and an American Diabetes Association mentorship award (to L. H. M.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
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