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The Control of the Metabolic Switch in Cancers by Oncogenes and Tumor
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TLDR
Cells from some tumors use an altered metabolic pattern compared with that of normal differentiated adult cells in the body, which provides substrates for cell growth and division and free energy (ATP) from enhanced glucose use.Abstract:
Cells from some tumors use an altered metabolic pattern compared with that of normal differentiated adult cells in the body. Tumor cells take up much more glucose and mainly process it through aerobic glycolysis, producing large quantities of secreted lactate with a lower use of oxidative phosphorylation that would generate more adenosine triphosphate (ATP), water, and carbon dioxide. This is the Warburg effect, which provides substrates for cell growth and division and free energy (ATP) from enhanced glucose use. This metabolic switch places the emphasis on producing intermediates for cell growth and division, and it is regulated by both oncogenes and tumor suppressor genes in a number of key cancer-producing pathways. Blocking these metabolic pathways or restoring these altered pathways could lead to a new approach in cancer treatments.read more
Citations
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Journal ArticleDOI
Molecular Biology of Liver Cancer
TL;DR: The characteristics and acquired capabilities of human primary liver cancer, based on the HCC-specific genetic and epigenetic alterations, are described and discussed.
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Queuine Micronutrient Deficiency Promotes Warburg Metabolism and Reversal of the Mitochondrial ATP Synthase in Hela Cells.
Patti Hayes,Claire Fergus,Magda Ghanim,Cansu Cirzi,Lyubomyr Burtnyak,Callum J. McGrenaghan,Francesca Tuorto,Derek P. Nolan,Vincent P. Kelly +8 more
TL;DR: The data suggest that queuosine hypomodification is a deliberate and advantageous adaptation of cancer cells to facilitate the metabolic switch between oxidative phosphorylation and aerobic glycolysis.
Journal ArticleDOI
Down-regulation of ACACA suppresses the malignant progression of Prostate Cancer through inhibiting mitochondrial potential.
Hui Zhang,Shaoyou Liu,Zhou-Da Cai,Dong Weimin,Jianheng Ye,Zhiduan Cai,Zhao-Dong Han,Yuxiang Liang,Yangjia Zhuo,Yong Luo,Xuejin Zhu,Yulin Deng,Yixun Zhang,Ren Liu,Yuanfa Feng,Jiarun Lai,Rui Zhou,Huijing Tan,Weide Zhong +18 more
TL;DR: Targeting ACACA gene and mitochondria might serve as a novel therapy for prostate cancer treatment as well as its effects on mitochondrial potential.
Book ChapterDOI
Targeting Altered Metabolism—Emerging Cancer Therapeutic Strategies
TL;DR: This chapter discusses the new understandings in cancer metabolism and the inhibitors being developed, which added new theoretical paradigms and new drug target proteins to the strategies for cancer therapy.
Journal ArticleDOI
Synergic chemoprevention with dietary carbohydrate restriction and supplementation of AMPK-activating phytochemicals: the role of SIRT1
Jong Doo Lee,Min-Ah Choi,Simon Weonsang Ro,Woo Ick Yang,Arthur Cho,Hye-Lim Ju,Sinhwa Baek,Sook In Chung,Won Jun Kang,Mijin Yun,Jeon Han Park +10 more
TL;DR: An isocaloric carbohydrate-restriction diet and natural AMPK-activating agents induce synergistic anticancer effects and SIRT1 acts as a tumor suppressor under a low-glucose condition in the transgenic liver cancer model developed by hydrodynamic transfection.
References
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Journal ArticleDOI
Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation
TL;DR: It is proposed that the metabolism of cancer cells, and indeed all proliferating cells, is adapted to facilitate the uptake and incorporation of nutrients into the biomass needed to produce a new cell.
Journal ArticleDOI
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.
Journal ArticleDOI
An Integrated Genomic Analysis of Human Glioblastoma Multiforme
D. Williams Parsons,Siân Jones,Xiaosong Zhang,Jimmy Lin,Rebecca J. Leary,Philipp Angenendt,Parminder Mankoo,Hannah Carter,I-Mei Siu,Gary L. Gallia,Alessandro Olivi,Roger E. McLendon,B.K. Ahmed Rasheed,Stephen T. Keir,Tatiana Nikolskaya,Yuri Nikolsky,Dana A. Busam,Hanna Tekleab,Luis A. Diaz,James Hartigan,Doug R. Smith,Robert L. Strausberg,Suely Kazue Nagahashi Marie,Sueli Mieko Oba Shinjo,Hai Yan,Gregory J. Riggins,Darell D. Bigner,Rachel Karchin,Nick Papadopoulos,Giovanni Parmigiani,Bert Vogelstein,Victor E. Velculescu,Kenneth W. Kinzler +32 more
TL;DR: Recurrent mutations in the active site of isocitrate dehydrogenase 1 (IDH1) occurred in a large fraction of young patients and in most patients with secondary GBMs and were associated with an increase in overall survival.
Journal ArticleDOI
IDH1 and IDH2 Mutations in Gliomas
Hai Yan,D. Williams Parsons,Genglin Jin,Roger E. McLendon,B.K. Ahmed Rasheed,Weishi Yuan,Ivan Kos,Ines Batinic-Haberle,Siân Jones,Gregory J. Riggins,Henry S. Friedman,Allan H. Friedman,David A. Reardon,James E. Herndon,Kenneth W. Kinzler,Victor E. Velculescu,Bert Vogelstein,Darell D. Bigner +17 more
TL;DR: Mutations of NADP(+)-dependent isocitrate dehydrogenases encoded by IDH1 and IDH2 occur in a majority of several types of malignant gliomas.