Increased UDP kinase activity in rat and human hepatomas

Abstract

PREVIOUS work1–4, (carried out in this laboratory with the molecular correlation concept as a conceptual and experimental approach resulted in an insight into the biochemical strategy of the cancer cell) much of it conducted with a model system of hepatomas of very different growth rates5, has revealed a gradually emerging metabolic imbalance that is linked with the increase in tumour growth rate1–4,6–12. Such biochemical alterations were manifested in progressive changes in the activities of opposing and competing key enzymes and opposing and competing metabolic pathways that correlated closely with tumour growth rate. These alterations in gene expression that seem to be linked with the increase in the expression of malignancy were manifested in increases in the activities of key glycolytic, pyrimidine and DNA synthesising enzymes4,7–12. Concurrently, there were progressive decreases in the activities of the key enzymes of gluconeogenesis, pyrimidine catabolism and the urea cycle4,7,8,10,12. In addition to this ‘malignancy-linked’ (growth-rate-linked) metabolic imbalance, we now show that the reprogramming of gene expression in cancer cells entails ‘transformation-linked’ alterations that are present in all hepatomas irrespective of growth rate or differentiation.