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J. Biol. Chem., Vol. 277, Issue 16, 14011-14019, April 19, 2002
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From the Hepatocyte nuclear factor 4
Analysis of Gene Expression Profile Induced by Hepatocyte Nuclear
Factor 4
in Hepatoma Cells Using an Oligonucleotide Microarray*
,§,
,,,
First Department of Internal Medicine and
the Department of Neurology and Psychiatry, Gifu University
School of Medicine, Gifu, Gifu 500-8705, Japan, the ¶ Laboratory
of Cellular Biochemistry, Department of Nutrition and Health
Science, Siebold University of Nagasaki, Nagayo, Nagasaki 851-2195, Japan, and the ** Institute of Applied Biochemistry, Yagi
Memorial Park, Mitake, Gifu 505-0116, Japan
(HNF-4), a
liver-specific transcription factor, plays a significant role in many
liver-specific functions, including lipid, glucose, drug, and ammonia
metabolism, and also in embryonal liver development. However, its
functions and regulation are not yet clearly understood. In this study, we constructed an adenovirus vector carrying rat HNF-4 cDNA and transfected the adenovirus to human hepatoma cells, HuH-7, to enforce
expression of the exogenous HNF-4 gene. We analyzed
HNF-4-induced genes using cDNA microarray technology, which included
over 9000 genes. As a result, 62 genes showed a greater than 2.0-fold
change in expression level after the viral transfection. Fifty-six
genes were consistently induced by HNF-4 overexpression, and six
genes were repressed. To assess HNF-4 function, we attempted to
classify the genes, which had been classified by their encoding protein functions in a previous report. We could classify 45 genes. The rest of
the HNF-4-sensitive genes were unclassified (4 genes) or not
identified (13 genes). Among the classified genes, almost half of the
induced genes (26 of 40) were related to metabolism genes and
particularly to lipid metabolism-related genes. This cDNA
microarray analysis showed that HNF-4 is one of the central liver
metabolism regulators.
*
This work was supported in part by Grant-in-aid 10670462 from the Ministry of Education, Culture, Sports, Science and Technology of Japan and by the Research Group of Intractable Liver Disease, sponsored by the Ministry of the Health, Labor, and Welfare of Japan.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.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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