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J. Biol. Chem., Vol. 277, Issue 41, 38930-38938, October 11, 2002
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From the The anticancer effects of
N-(4-hydroxyphenyl)retinamide (4HPR), a potential
chemopreventive or chemotherapeutic retinamide, are thought to be
derived from its ability to induce apoptosis. However, the
mechanism of apoptosis induced by 4HPR remains unclear. Thus, this
study was designed to identify the gene(s) responsible for induction of
apoptosis by 4HPR. Apoptosis was effectively induced by
4HPR in human hepatoma cells. Using the differential display-PCR
method, a gene involved in the response to 4HPR was identified, and
cells in which the expression of that gene was modulated were analyzed
for survival, induction of apoptosis, and cell cycle.
GADD153, a gene involved in growth arrest and apoptosis,
was preferentially expressed in human hepatoma cells as well as in
other cancer cells during 4HPR-induced apoptosis. 4HPR regulates
GADD153 expression at the post-transcriptional level in Hep
3B cells and at the transcriptional and post-transcriptional levels in
SK-HEP-1 cells, when assayed by in vitro transfection and
mRNA stability experiments. To determine the role of the GADD153 protein overexpression that is induced by 4HPR, Hep 3B cells with ectopic overexpression of GADD153 were found to be growth-arrested (at
G1) and readily underwent apoptosis following
treatment with 4HPR or even when they reached confluence.
N-Acetyl-L-cysteine or GADD153
antisense significantly protected the cells from 4HPR-induced apoptosis, accompanying by the inhibition of GADD153
overexpression. Parthenolide-mediated overexpression of GADD153
resulted in enhanced 4HPR-induced apoptosis. These results
suggest that GADD153 overexpression induced by 4HPR may contribute to
the anticancer effects (induction of apoptosis and growth arrest)
of 4HPR on cancer cells.
GADD153-mediated Anticancer Effects of
N-(4-Hydroxyphenyl)retinamide on Human Hepatoma Cells*
§,,, Division of Gastroenterology and Hepatology,
Department of Internal Medicine, Institute for Molecular Biology and
Genetics, Chonbuk National University Medical School and Hospital,
Chonju, Chonbuk 561-712 and the ¶ ICLAS Monitoring Subcenter
Korea, Korea Research Institute of Bioscience and Biotechnology, Taejon
305-600, South Korea
*
This work was supported by the 21C Frontier Human Genome
Project grant.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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