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Metabolic adaptation to cancer growth: From the cell to the organism

机译:代谢适应癌症生长:从细胞到生物体

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Tumour cells proliferate much faster than normal cells; nearly all anticancer treatments are toxic to both cell types, limiting their efficacy. The altered metabolism resulting from cellular transformation and cancer progression supports cellular proliferation and survival, but leaves cancer cells dependent on a continuous supply of energy and nutrients. Hence, many metabolic enzymes have become targets for new cancer therapies. In addition to its well-described roles in cell-cycle progression and cancer, the cyclin/CDK-pRB-E2F1 pathway contributes to lipid synthesis, glucose production, insulin secretion, and glycolytic metabolism, with strong effects on overall metabolism. Notably, these cell-cycle regulators trigger the adaptive "metabolic switch" that underlies proliferation. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
机译:肿瘤细胞比正常细胞更快地增殖; 几乎所有抗癌治疗都对两种细胞类型有毒,限制了它们的功效。 由细胞转化和癌症进展引起的改变的代谢支持细胞增殖和生存,但留下癌细胞依赖于连续供应能量和营养素。 因此,许多代谢酶已成为新癌症疗法的靶标。 除了其在细胞周期进展和癌症中的良好作用之外,细胞周期蛋白/ CDK-PRB-E2F1途径有助于脂质合成,葡萄糖生产,胰岛素分泌和糖酵解代谢,对整体代谢产生很强的影响。 值得注意的是,这些细胞周期调节器触发了潜在的增殖的“代谢开关”。 (c)2014年Elsevier Ireland Ltd.保留所有权利。

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