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(Received for publication, November 28, 1995, and in revised form, August 8, 1996)
From the Exposure to ionizing radiation leads to induction
of the immediate-early gene, early growth response-1
(Egr-1). Previous studies have suggested distinct cell
type- and inducer-specific roles for EGR-1 protein in cellular growth
inhibition. The present study was undertaken to determine the
functional role of EGR-1 in growth inhibition caused by exposure of
tumor cells to ionizing radiation. Exposure to ionizing radiation
caused induction of EGR-1 protein in human melanoma cells A375-C6.
Inhibition of either the function of EGR-1 protein by stable
transfection with a dominant-negative mutant or the expression of EGR-1
by transient transfection with an antisense oligomer resulted in a
diminished growth-inhibitory response to ionizing radiation. Because
previous studies have suggested that mutations in the tumor-suppressor
gene p53 confer radio-resistance, we examined the p53 status of A375-C6
cells. Interestingly, both the parental and the transfected A375-C6
cells showed trisomy for wild-type p53 alleles. Exposure to ionizing radiation resulted in induction of p53 protein that localized to the
nucleus in A375-C6 cells. These data suggest that inhibition of EGR-1
function confers radio resistance despite the induction of wild-type
nuclear p53. Thus, EGR-1 is required for the growth-inhibitory response
to ionizing radiation in A375-C6 cells.
Volume 271, Number 46,
Issue of November 15, 1996
pp. 29231-29237
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.
,
,
,¶
and
Department of Radiation Medicine, the
§ Department of Surgery,
Department of Microbiology and Immunology,
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