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One of the most characteristic phenotypes of rapidly growing
cancer cells is their propensity to catabolize glucose at high rates.
Type II hexokinase, which is expressed at high levels in such cells and
bound to the outer mitochondrial membrane, has been implicated as a
major player in this aberrant metabolism. Here we report the isolation
and sequence of a 4.3-kilobase pair proximal promoter region of the
Type II hexokinase gene from a rapidly growing, highly glycolytic
hepatoma cell line (AS-30D). Analysis of the sequence enabled the
identification of putative promoter elements, including a TATA box, a
CAAT element, several Sp-1 sites, and response elements for glucose,
insulin, cAMP, Ap-1, and a number of other factors. Transfection
experiments with AS-30D cells showed that promoter activity was
enhanced 3.4-, 3.3-, 2.4-, 2.1-, and 1.3-fold, respectively, by
glucose, phorbol 12-myristate 13-acetate (a phorbol ester), insulin,
cAMP, and glucagon. In transfected hepatocytes, these same agents
produced little or no effect. The results emphasize normal versus tumor cell differences in the regulation of Type II hexokinase and
indicate that transcription of the Type II tumor gene may occur
independent of metabolic state, thus, providing the cancer cell with a
selective advantage over its cell of origin.
Volume 270,
Number 28,
Issue of July 14, pp. 16918-16925, 1995
©1995 by The American Society for Biochemistry and Molecular Biology, Inc.
ISOLATION, SEQUENCE, AND ACTIVITY OF THE PROMOTER FOR TYPE II
HEXOKINASE
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