The biology of cancer: metabolic reprogramming fuels cell growth and proliferation
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TLDR
This review examines the idea that several core fluxes, including aerobic glycolysis, de novo lipid biosynthesis, and glutamine-dependent anaplerosis, form a stereotyped platform supporting proliferation of diverse cell types and regulates regulation of these fluxes by cellular mediators of signal transduction and gene expression.About:
This article is published in Cell Metabolism.The article was published on 2008-01-01 and is currently open access. It has received 3526 citations till now. The article focuses on the topics: PI3K/AKT/mTOR pathway & Lipid biosynthesis.read more
Citations
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ACLY facilitates colon cancer cell metastasis by CTNNB1
Jun Wen,Xuejie Min,Mengqin Shen,Qian Hua,Yuan Han,Li Zhao,Liu Liu,Gang Huang,Jianjun Liu,Xiaoping Zhao +9 more
TL;DR: Immunohistochemical analysis of 78 colon cancer patients showed that the high expression levels of ACLY and CTNNB1 protein was positively correlated with metastasis of colon cancer, shedding new light on the molecular mechanism underlying colon cancer metastasis, which might help in improving therapeutic efficacy.
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Endothelial cell metabolism: parallels and divergences with cancer cell metabolism
TL;DR: These studies show that metabolic pathways in endothelial cells (ECs) importantly regulate angiogenesis in conjunction with genetic signals, and emerging insights in EC metabolism are highlighted and discussed in perspective of cancer cell metabolism.
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Light Exposure at Night Disrupts Host/Cancer Circadian Regulatory Dynamics: Impact on the Warburg Effect, Lipid Signaling and Tumor Growth Prevention
David E. Blask,Robert T. Dauchy,Erin M. Dauchy,Lulu Mao,Steven M. Hill,Michael W. Greene,Victoria P. Belancio,Leonard A. Sauer,Leslie L. Davidson +8 more
TL;DR: It is determined that circulating systemic factors in the host and the Warburg effect, linoleic acid uptake/metabolism and growth signaling activities in the tumor are dynamically regulated, coordinated and integrated within circadian time structure over a 24-hour light/dark cycle by SCN-driven nocturnal pineal production of the anticancer hormone melatonin.
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p53 and metabolism: from mechanism to therapeutics.
Fernando Moreira Simabuco,Mirian Galliote Morale,Isadora Carolina Betim Pavan,Ana Paula Morelli,Fernando R Silva,Rodrigo Esaki Tamura +5 more
TL;DR: The interplay between p53 and metabolism is essential in the decision of cell fate and for cancer therapeutics and drugs that target metabolism may have different outcomes and metabolism may modulate drug resistance.
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The metabolic landscape of RAS-driven cancers from biology to therapy
TL;DR: Mukhopadhyay et al. as mentioned in this paper discuss the metabolic reprogramming mediated by oncogenic RAS in cancer and elucidate the underlying mechanisms that could translate to novel therapeutic opportunities to target metabolic vulnerabilities in RAS-driven cancers.
References
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Dennis J. Slamon,William Godolphin,Lovell A. Jones,John A. Holt,Steven G. Wong,Duane E. Keith,Wendy J. Levin,Susan G. Stuart,Judy Udove,Axel Ullrich,Michael F. Press +10 more
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Targeting HIF-1 for cancer therapy
TL;DR: Hypoxia-inducible factor 1 (HIF-1) activates the transcription of genes that are involved in crucial aspects of cancer biology, including angiogenesis, cell survival, glucose metabolism and invasion.
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High frequency of mutations of the PIK3CA gene in human cancers
Yardena Samuels,Zhenghe Wang,Alberto Bardelli,Natalie Silliman,Janine Ptak,Steve Szabo,Hai Yan,Adi F. Gazdar,Steven M. Powell,Gregory J. Riggins,James K V Willson,Sanford D. Markowitz,Kenneth W. Kinzler,Bert Vogelstein,Victor E. Velculescu +14 more
TL;DR: To determine if PI3Ks are genetically altered in tumorigenesis, they were sequenced in human for the first time and the results allowed us to assess the importance of phosphatidylinositol 3-kinases in neoplasia.
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HIF-1-mediated expression of pyruvate dehydrogenase kinase: A metabolic switch required for cellular adaptation to hypoxia
TL;DR: A hypoxia-induced metabolic switch that shunts glucose metabolites from the mitochondria to glycolysis to maintain ATP production and to prevent toxic ROS production is revealed.