Energy Homeostasis and Cancer Prevention: The AMP-Activated Protein Kinase

被引:70
作者
Fay, Judith R. [1 ]
Steele, Vernon [2 ]
Crowell, James A. [3 ]
机构
[1] CCS Associates, Mountain View, CA 94043 USA
[2] NCI, Chemoprevent Agent Dev Res Grp, Canc Prevent Div, NIH, Bethesda, MD 20892 USA
[3] NCI, Dev Therapeut Program, Div Canc Treatment & Diag, NIH, Bethesda, MD 20892 USA
关键词
FATTY-ACID SYNTHASE; ACETYL-COA-CARBOXYLASE; METABOLIC SYNDROME; MAMMALIAN TARGET; CALORIE RESTRICTION; CELL-GROWTH; IN-VIVO; METFORMIN; PATHWAY; INSULIN;
D O I
10.1158/1940-6207.CAPR-08-0166
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Caloric restriction has long been recognized as an extremely effective cancer preventive. Current population demographics suggest that caloric excess and obesity will lead to increased cancer incidence, underscoring the need to elucidate the molecular mechanisms that couple dysregulated energy homeostasis to aberrant cell growth. The AMP-activated protein kinase (AMPK) is a critical monitor of cellular energy status, largely studied for its importance in metabolic regulation. AMPK also controls processes relevant to tumor development, including cell cycle progression, protein synthesis, cell growth, and survival. Several tumor suppressors impinge on AMPK signaling, and activation of the kinase inhibits tumor growth. However, AMPK can also promote cancer in some settings, necessitating a more complete understanding of the complexities of this signaling network. Because dysregulated energy balance is a nexus for multiple chronic diseases of aging, drugs that target these pathways may find broad utility in aging populations.
引用
收藏
页码:301 / 309
页数:9
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