Cancer Cell Metabolism: Change of Gene Expression to Induce Proliferation in Some Cancer Cells

Cody Hartman


As one of the ten hallmarks of cancer, the deregulation of the metabolic processes in cancer cells is crucial for growth and proliferation. First demonstrated by Otto Warburg (1924), cancer cells alter their metabolism to an energetically inefficient catabolic processing of glucose. This process, now known as the Warburg effect, can only generate ~2 ATP per glucose molecule in comparison to the normal generation of ~32 ATP through normal catabolic processing. However, differential gene expression in cancer cells account for the lacking energy generation with changes in stringent response, non-essential amino acid uptake, and increased glucose uptake among many factors. Lactate, the alternative product of glycolysis (in comparison to pyruvate) can be used as an alternative indirect carbon source in the TCA cycle with an increased efficiency over the glucose counterpart. Glutaminolysis, a prominent secondary metabolic pathway of cancer cells, uptakes glutamine from the environment to be used for processing of secondary metabolites as well as cell signaling. Recent research progress has shown the need for glutamine in cancerous cells as well as targeted treatment to disallow the use of glutamine by tumor cells. As exemplified, there are many pathways of cancer cells that are differentially changed for the sole purpose of growth and proliferation. In this review, the regulation of glucose uptake as well as the non-essential amino acid Glutamine will be discussed. With understanding of these pathways, inhibitors and other treatments can be hypothesized to assist in inhibiting proliferation of malignant cells. 

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