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pubmed-article:18818743pubmed:abstractTextTo explore the metabolic effects of Bcl-2 in tumor cells, a stable clone of HuH-7/bcl-2 and its control HuH-7/neo were established. Mitochondrial localization of ectopic Bcl-2 was demonstrated both by western blotting and immunofluorescence. HuH-7/bcl-2 cells consumed glucose at a higher rate, exhausted the available cellular ATP and died on day 9, while HuH-7/neo cells were still alive for 10 days under the same condition where cells were cultured without replenishment of the medium. The expression of the hexokinase II gene was up-regulated in HuH-7/bcl-2 at its protein level. Taken together, we suggest that the forced expression of Bcl-2 in human hepatoma may cause the cells to become more glucose-dependent for survival.lld:pubmed
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pubmed-article:18818743pubmed:authorpubmed-author:ShidojiYoshih...lld:pubmed
pubmed-article:18818743pubmed:authorpubmed-author:OkamotoKyokoKlld:pubmed
pubmed-article:18818743pubmed:authorpubmed-author:MuraguchiTaka...lld:pubmed
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pubmed-article:18818743pubmed:volume43lld:pubmed
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pubmed-article:18818743pubmed:pagination101-8lld:pubmed
pubmed-article:18818743pubmed:year2008lld:pubmed
pubmed-article:18818743pubmed:articleTitleEnhanced Glucose Requirement in Human Hepatoma-derived HuH-7 Cells by Forced Expression of the bcl-2 Gene.lld:pubmed
pubmed-article:18818743pubmed:affiliationMolecular & Cellular Biology, Graduate School of Human Health Sciences, Siebold University of Nagasaki, Academy Hills 1-1-1, Nagayo, Nagasaki 851-2195, Japan.lld:pubmed
pubmed-article:18818743pubmed:publicationTypeJournal Articlelld:pubmed