Regulation of Cancer Metabolism by Oncogenes and Tumor Suppressors

被引:85
作者
Iurlaro, Raffaella [1 ]
Lucia Leon-Annicchiarico, Clara [1 ]
Munoz-Pinedo, Cristina [1 ]
机构
[1] Bellvitge Biomed Res Inst IDIBELL, Cell Death Regulat Grp, Barcelona, Spain
来源
CONCEPTUAL BACKGROUND AND BIOENERGETIC/MITOCHONDRIAL ASPECTS OF ONCOMETABOLISM | 2014年 / 542卷
关键词
NF-KAPPA-B; ACTIVATED PROTEIN-KINASE; NOVO PYRIMIDINE SYNTHESIS; PEUTZ-JEGHERS-SYNDROME; INDUCIBLE FACTOR-I; MTOR COMPLEX 1; C-MYC; GLUTAMINE-METABOLISM; GENE-EXPRESSION; CELL-CYCLE;
D O I
10.1016/B978-0-12-416618-9.00003-0
中图分类号
Q5 [生物化学];
学科分类号
070307 [化学生物学];
摘要
Cell proliferation requires the coordination of multiple signaling pathways as well as the provision of metabolic substrates. Nutrients are required to generate such building blocks and their form of utilization differs to significant extents between malignant tissues and their nontransformed counterparts. Thus, oncogenes and tumor suppressor genes regulate the proliferation of cancer cells also by controlling their metabolism. Here, we discuss the central anabolic functions of the signaling pathways emanating from mammalian target of rapamycin, MYC, and hypoxia-inducible factor-1. Moreover, we analyze how oncogenic proteins like phosphoinositide-3-kinase, AKT, and RAS, tumor suppressors such as phosphatase and tensin homolog, retinoblastoma, and p53, as well as other factors associated with the proliferation or survival of cancer cells, such as NF-kappa B, regulate cellular metabolism.
引用
收藏
页码:59 / 80
页数:22
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