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Open AccessJournal ArticleDOI

5-Aminoimidazole-4-carboxamide-1-β-D-ribofuranoside Inhibits Cancer Cell Proliferation in Vitro and in Vivo via AMP-activated Protein Kinase

TLDR
Results indicate that AICAR can be utilized as a therapeutic drug to inhibit cancer, and AMPK can be a potential target for treatment of various cancers independent of the functional tumor suppressor gene, LKB.
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This article is published in Journal of Biological Chemistry.The article was published on 2005-11-25 and is currently open access. It has received 346 citations till now. The article focuses on the topics: AMPK & AMP-activated protein kinase.

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Citations
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Journal ArticleDOI

AMP-activated/SNF1 protein kinases: conserved guardians of cellular energy.

TL;DR: Surprisingly, recent results indicate that the AMPK system is also important in functions that go beyond the regulation of energy homeostasis, such as the maintenance of cell polarity in epithelial cells.
Journal ArticleDOI

Insulin and insulin-like growth factor signalling in neoplasia

TL;DR: Epidermiological, clinical and laboratory research methods are being used to investigate novel cancer prevention and treatment strategies related to insulin and IGF signalling, including the use of novel receptor-specific antibodies, receptor kinase inhibitors and AMP-activated protein kinase activators.
Journal ArticleDOI

AMPK in Health and Disease

TL;DR: This review looks at how AMPK integrates stress responses such as exercise as well as nutrient and hormonal signals to control food intake, energy expenditure, and substrate utilization at the whole body level and the possible role of AMPK in multiple common diseases.
Journal ArticleDOI

AMP-Activated Protein Kinase in Metabolic Control and Insulin Signaling

TL;DR: Although it may have evolved to respond to metabolic stress at the cellular level, hormones and cytokines such as insulin, leptin, and adiponectin can interact with the system, and it now appears to play a key role in maintaining energy balance at the whole body level.
Journal ArticleDOI

Metformin Inhibits Mammalian Target of Rapamycin–Dependent Translation Initiation in Breast Cancer Cells

TL;DR: Results show that metformin-mediated AMPK activation leads to inhibition of mTOR and a reduction in translation initiation, thus providing a possible mechanism of action of meetformin in the inhibition of cancer cell growth.
References
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Journal ArticleDOI

WAF1, a potential mediator of p53 tumor suppression

TL;DR: A gene is identified, named WAF1, whose induction was associated with wild-type but not mutant p53 gene expression in a human brain tumor cell line and that could be an important mediator of p53-dependent tumor growth suppression.
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Adiponectin stimulates glucose utilization and fatty-acid oxidation by activating AMP-activated protein kinase

TL;DR: It is shown that phosphorylation and activation of the 5′-AMP-activated protein kinase (AMPK) are stimulated with globular and full-length Ad in skeletal muscle and only with full- lengths Ad in the liver, indicating that stimulation of glucose utilization and fatty-acid oxidation by Ad occurs through activation of AMPK.
Journal ArticleDOI

TSC2 mediates cellular energy response to control cell growth and survival.

TL;DR: It is described that TSC2 is regulated by cellular energy levels and plays an essential role in the cellular energy response pathway and its phosphorylation by AMPK protect cells from energy deprivation-induced apoptosis.
Book ChapterDOI

de la Chapelle, A.

TL;DR: De la Chapelle dysplasia, also known as atelosteogenesis type II, is a lethal form of neonatal dwarfism in which gross limb shortening is associated with a characteristic triangular configuration of the radius and ulna.
Journal ArticleDOI

Leptin stimulates fatty-acid oxidation by activating AMP-activated protein kinase.

TL;DR: It is shown that leptin selectively stimulates phosphorylation and activation of the α2 catalytic subunit of AMPK (α2 AMPK) in skeletal muscle, thus establishing a previously unknown signalling pathway for leptin, and identifying AMPK as a principal mediator of the effects of leptin on fatty-acid metabolism in muscle.
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