Although significant progress has been made in the diagnosis and treatment of
gastric cancer, the overall survival rate of the disease remains unchanged at approximately 20%-25%. Thus, there is an urgent need for a better understanding of the molecular biology aspects of the disease in the hope of discovering novel diagnosis and treatment strategies. Recent years have witnessed decisive roles of aberrant
cancer cell metabolism in the maintenance of malignant hallmarks of
cancers, and
cancer cell metabolism has been regarded as a novel target for the treatment of
cancer. CDK2, a cell cycle-dependent
kinase that usually regulates cell cycle progression and the DNA damage response, is reported to be upregulated in many
cancers. However, little is known about its role in
cancer cell metabolism. In the present study, we showed that silencing CDK2 inhibited the aerobic glycolytic capacity of
gastric cancer cell lines. Mechanism explorations showed that silencing CDK2 increased expression of the SIRT5
tumor suppressor. In addition, the physiological roles of SIRT5 in the regulation of proliferation and glycolysis were studied in
gastric cancer cells. Taken together, the present study uncovered novel roles of the CDK2/SIRT5 axis in
gastric cancer and suggests future studies concerning
gastric cancer cell metabolism.