Targeting energy metabolic and oncogenic signaling pathways in triple-negative breast cancer by a novel adenosine monophosphate-activated protein kinase (AMPK) activator.
Kuen Haur Lee,En-Chi Hsu,Jih-Hwa Guh,Hsiao-Ching Yang,Dasheng Wang,Samuel K. Kulp,Charles L. Shapiro,Ching-Shih Chen +7 more
TLDR
OSU-53 is a potent, orally bioavailable AMPK activator that acts through a broad spectrum of antitumor activities downstream of AMPK activation and modulated relevant intratumoral biomarkers of drug activity.About:
This article is published in Journal of Biological Chemistry.The article was published on 2011-11-11 and is currently open access. It has received 95 citations till now. The article focuses on the topics: AMPK & Protein kinase B.read more
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AMPK: guardian of metabolism and mitochondrial homeostasis.
Sébastien Herzig,Reuben J. Shaw +1 more
TL;DR: How AMPK functions as a central mediator of the cellular response to energetic stress and mitochondrial insults and coordinates multiple features of autophagy and mitochondrial biology is discussed.
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AMP-activated protein kinase: new regulation, new roles?
TL;DR: The present review examines the recent progress aimed at understanding the regulation of AMPK and discusses some of the latest developments that have emerged in key areas of human physiology where AMPK is thought to play an important role.
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The AMP-activated protein kinase (AMPK) and cancer: Many faces of a metabolic regulator
TL;DR: The contextual nature of the "two faces" of AMPK in cancer is discussed, and the rationale and context for employing AMPK activators versus inhibitors for cancer therapy is discussed.
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Hypoxia-inducing factors as master regulators of stemness properties and altered metabolism of cancer- and metastasis-initiating cells.
TL;DR: The targeting of HIF signalling network and altered metabolic pathways represents new promising strategies to eradicate the total mass of cancer cells and improve the efficacy of current therapies against aggressive and metastatic cancers and prevent disease relapse.
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Metformin: Multi-faceted protection against cancer
Sonia Del Barco,Alejandro Vazquez-Martin,Sílvia Cufí,Cristina Oliveras-Ferraros,Joaquim Bosch-Barrera,Jorge Joven,Begoña Martin-Castillo,Javier A. Menendez +7 more
TL;DR: Current and future clinical trials will elucidate whether metformin has the potential to be used in preventive and treatment settings as an adjuvant to current cancer therapeutics, and preliminary evidence that met formin may regulate cellular senescence, an innate safeguard against cellular immortalization.
References
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The basics of epithelial-mesenchymal transition
Raghu Kalluri,Robert A. Weinberg +1 more
TL;DR: Processes similar to the EMTs associated with embryo implantation, embryogenesis, and organ development are appropriated and subverted by chronically inflamed tissues and neoplasias and the identification of the signaling pathways that lead to activation of EMT programs during these disease processes is providing new insights into the plasticity of cellular phenotypes.
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Role of AMP-activated protein kinase in mechanism of metformin action
Gaochao Zhou,Robert W. Myers,Ying Li,Yuli Chen,Xiaolan Shen,Judy Fenyk-Melody,Margaret Wu,John Ventre,Thomas W. Doebber,Nobuharu Fujii,Nicolas Musi,Michael F. Hirshman,Laurie J. Goodyear,David E. Moller +13 more
TL;DR: It is reported that metformin activates AMPK in hepatocytes; as a result, acetyl-CoA carboxylase (ACC) activity is reduced, fatty acid oxidation is induced, and expression of lipogenic enzymes is suppressed.
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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.
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AMP-activated protein kinase: Ancient energy gauge provides clues to modern understanding of metabolism
TL;DR: Through signaling, metabolic, and gene expression effects, AMPK enhances insulin sensitivity and fosters a metabolic milieu that may reduce the risk for obesity and type 2 diabetes.
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The transcription factor snail is a repressor of E-cadherin gene expression in epithelial tumour cells.
Eduard Batlle,Elena Sancho,Clara Francí,David Domı́nguez,Mercè Monfar,Josep Baulida,Antonio García de Herreros +6 more
TL;DR: It is shown that the transcription factor Snail, which is expressed by fibroblasts and some E-cadherin-negative epithelial tumour cell lines, binds to three E-boxes present in the human E-CADherin promoter and represses transcription of E- cadhersin.