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J Biol Chem, Vol. 274, Issue 48, 34186-34195, November 26, 1999
From the a Albert Einstein Cancer Center,
f Department of Medicine, b Department of Developmental
and Molecular Biology, and g Department of Cell Biology, Albert
Einstein College of Medicine, Bronx, New York 10461, the
h Institut Curie, INSERM U 255, 26 rue d'Ulm,
F-75005 Paris, France, the i Department of Microbiology,
University of Buffalo School of Medicine, Buffalo, New York 14214, and the j Department of Microbiology, Immunology, and the Lurie
Cancer Center, Northwestern University Medical School,
Chicago, Illinois 60611
The adenovirus E1A protein interferes with
regulators of apoptosis and growth by physically interacting with cell
cycle regulatory proteins including the retinoblastoma tumor suppressor
protein and the coactivator proteins p300/CBP (where CBP is the
CREB-binding protein). The p300/CBP proteins occupy a pivotal role in
regulating mitogenic signaling and apoptosis. The mechanisms by which
cell cycle control genes are directly regulated by p300 remain to be determined. The cyclin D1 gene, which is overexpressed in
many different tumor types, encodes a regulatory subunit of a
holoenzyme that phosphorylates and inactivates PRB. In the present
study E1A12S inhibited the cyclin D1 promoter via the amino-terminal p300/CBP binding domain in human choriocarcinoma JEG-3 cells. p300
induced cyclin D1 protein abundance, and p300, but not CBP, induced the
cyclin D1 promoter. cyclin D1 or p300 overexpression inhibited
apoptosis in JEG-3 cells. The CH3 region of p300, which was required
for induction of cyclin D1, was also required for the inhibition of
apoptosis. p300 activated the cyclin D1 promoter through an activator
protein-1 (AP-1) site at
Activation of the cyclin D1 Gene by the
E1A-associated Protein p300 through AP-1 Inhibits Cellular
Apoptosis
954 and was identified within a DNA-bound
complex with c-Jun at the AP-1 site. Apoptosis rates of embryonic
fibroblasts derived from mice homozygously deleted of the cyclin
D1 gene (cyclin D1
/) were
increased compared with wild type control on several distinct matrices.
p300 inhibited apoptosis in cyclin D1+/+
fibroblasts but increased apoptosis in cyclin
D1/ cells. The anti-apoptotic
function of cyclin D1, demonstrated by sub-G1 analysis and
annexin V staining, may contribute to its cellular transforming and
cooperative oncogenic properties.
Copyright © 1999 by The American Society for Biochemistry and Molecular Biology, Inc.
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