The Biology of Cancer: Metabolic Reprogramming Fuels Cell Growth and Proliferation

Understanding the Intersections between Metabolism and Cancer Biology

Biology of glucose metabolization in cancer cells

Cancer is a disease at the cellular level involving heritable disorders in cellular control mechanism. Cancer cells also need to adapt their metabolism to survive and multiply under the metabolically compromised conditions provided by the tumor microenvironment. Tumor cells alter their metabolism to maintain unregulated cellular proliferation and survival, but this transformation leaves them reliant on constant supply of nutrients and energy. They alter their metabolism to support their rapid proliferation and expansion across the body. After the discovery of based on the altered cancer cell metabolism in 1930, loads of studies have shed light on several aspects of cancer metabolism with a common goal to find new ways for effectively eliminating tumor cells by targeting their energy metabolism. Research has directed most of its resources to elucidate the causes, prevention and possible cure for cancer, yet the process has been elusive claiming human lives more than ever. This disease is a manifestation of etiological and pathological disturbances of mechanisms that control cell division, differentiation and metabolism. 50% of all human tumors carry genetic alterations that lead to the inactivation of some tumor suppressor proteins. Cancer cells are shown to experience characteristic changes in their metabolic programs, including increased uptake of glucose, enhanced rates of glutaminolysis and fatty acids synthesis, suggesting that metabolic shifts supports tumor cells growth and survival. In this review, we summarized the major concepts of glucose metabolization and explore the molecular basis of aerobic glycolysis of cancer cells.

Hallmarks of Cancer: The Next Generation

The hallmarks of cancer comprise six biological capabilities acquired during the multistep development of human tumors. The hallmarks constitute an organizing principle for rationalizing the complexities of neoplastic disease. They include sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, and activating invasion and metastasis. Underlying these hallmarks are genome instability, which generates the genetic diversity that expedites their acquisition, and inflammation, which fosters multiple hallmark functions. Conceptual progress in the last decade has added two emerging hallmarks of potential generality to this list-reprogramming of energy metabolism and evading immune destruction. In addition to cancer cells, tumors exhibit another dimension of complexity: they contain a repertoire of recruited, ostensibly normal cells that contribute to the acquisition of hallmark traits by creating the "tumor microenvironment." Recognition of the widespread applicability of these concepts will increasingly affect the development of new means to treat human cancer.