Enhanced glucose requirement in human hepatoma-derived HuH-7 cells by forced expression of the bcl-2 gene

Abstract

To 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.