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Molecular and Cellular Biology, January 2000, p. 233-241, Vol. 20, No. 1
0270-7306/0/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
ei24, a p53 Response Gene Involved in Growth
Suppression and Apoptosis
Zhengming
Gu,1
Cathy
Flemington,2
Thomas
Chittenden,2 and
Gerard P.
Zambetti1,3,*
Department of Biochemistry, St. Jude
Children's Research Hospital, Memphis, Tennessee
381051; Department of Biochemistry,
University of Tennessee, Memphis Tennessee
381633; and Apoptosis Technology,
Inc., Cambridge, Massachusetts 021392
Received 26 August 1999/Returned for modification 24 September
1999/Accepted 7 October 1999
DNA damage and/or hyperproliferative signals activate the wild-type
p53 tumor suppressor protein, which induces a G1 cell cycle
arrest or apoptosis. Although the mechanism of p53-mediated cell cycle
arrest is fairly well defined, the p53-dependent pathway regulating
apoptosis is poorly understood. Here we report the functional
characterization of murine ei24 (also known as
PIG8), a gene directly regulated by p53, whose
overexpression negatively controls cell growth and induces apoptotic
cell death. Ectopic ei24 expression markedly inhibits cell
colony formation, induces the morphological features of apoptosis, and
reduces the number of
-galactosidase-marked cells, which is
efficiently blocked by coexpression of Bcl-XL. The
ei24/PIG8 gene is localized on human chromosome
11q23, a region frequently altered in human cancers. These results
suggest that ei24 may play an important role in negative
cell growth control by functioning as an apoptotic effector of p53
tumor suppressor activities.
*
Corresponding author. Mailing address: Department of
Biochemistry, St. Jude Children's Research Hospital, 332 North
Lauderdale, Memphis, TN 38105. Phone: (901) 495-3429. Fax: (901)
525-8025. E-mail: gerard.zambetti{at}stjude.org.
Molecular and Cellular Biology, January 2000, p. 233-241, Vol. 20, No. 1
0270-7306/0/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
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