The aim of the work was to evaluate whether or not there is glycolytic reprogramming in the neighboring cells of
colorectal cancer (CRC). Using postoperative material we have compared the functional capacity of oxidative phosphorylation (OXPHOS) in CRC cells, their glycolytic activity and their inclination to aerobic glycolysis, with those of the surrounding and healthy colon tissue cells. Experiments showed that human CRC cannot be considered a hypoxic
tumor, since the
malignancy itself and cells surrounding it exhibited even higher rates of OXPHOS than healthy large intestine. The absence of acute
hypoxia in
colorectal carcinomas was also confirmed by their practically equal
glucose-phosphorylating capacity as compared with surrounding non-tumorous tissue and by upregulation of
VEGF family and their
ligands. Studies indicated that human CRC cells in vivo exert a strong distant effect on the energy metabolism of neighboring cells, so that they acquire the bioenergetic parameters specific to the
tumor itself. The growth of
colorectal carcinomas was associated with potent downregulation of the
creatine kinase system. As compared with healthy colon tissue, the
tumor surrounding cells display upregulation of OXPHOS and have high values of basal and
ADP activated respiration rates. Strong differences between the normal and CRC cells in the affinity of their mitochondria for
ADP were revealed; the corresponding Km values were measured as 93.6±7.7 µM for CRC cells and 84.9±9.9 µM for nearby tissue; both these apparent Km (
ADP) values were considerably (by almost 3 times) lower in comparison with healthy colon tissue cells (256±34 µM).