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Critical Reviews™ in Eukaryotic Gene Expression
インパクトファクター: 1.841 5年インパクトファクター: 1.927 SJR: 0.649 SNIP: 0.516 CiteScore™: 1.96

ISSN 印刷: 1045-4403
ISSN オンライン: 2162-6502

Critical Reviews™ in Eukaryotic Gene Expression

DOI: 10.1615/CritRevEukarGeneExpr.v22.i1.20
pages 17-35

Carbon Source Metabolism and Its Regulation in Cancer Cells

Chengqian Yin
Department of Biology, College of Arts and Sciences, Drexel University, Philadelphia, Pennsylvania
Shuo Qie
Department of Biology, College of Arts and Sciences, Drexel University; Department of Pathology and Laboratory Medicine, Drexel University College of Medicine, Philadelphia, Pennsylvania
Nianli Sang
Department of Biology, College of Arts and Sciences, Drexel University; Department of Pathology and Laboratory Medicine, Drexel University College of Medicine, Philadelphia, Pennsylvania

要約

Cancer cell proliferation and progression require sufficient supplies of nutrients including carbon sources, nitrogen sources, and molecular oxygen. Particularly, carbon sources and molecular oxygen are critical for the generation of ATP and building blocks, and for the maintenance of intracellular redox status. However, solid tumors frequently outgrow the blood supply, resulting in nutrient insufficiency. Accordingly, cancer cell metabolism shows aberrant biochemical features that are consequences of oncogenic signaling and adaptation. Those adaptive metabolism features, including the Warburg effect and addiction to glutamine, may form the biochemical basis for resistance to chemotherapy and radiation. A better understanding of the regulatory mechanisms that link the signaling pathways to adaptive metabolic reprogramming may identify novel biomarkers for drug development. In this review, we focus on the regulation of carbon source utilization at a cellular level, emphasizing its relevance to proliferative biosynthesis in cancer cells. We summarize the essential needs of proliferating cells and the metabolic features of glucose, lipids, and glutamine, and we review the roles of transcription regulators (i.e., HIF-1, c-Myc, and p53) and two major oncogenic signaling pathways (i.e., PI3K-Akt and MAPK) in regulating the utilization of carbon sources. Finally, the effects of glucose on cell proliferation and perspective from both biochemical and cellular angles are discussed.


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