Fundamentals of cancer metabolism
TLDR
A conceptual framework to understand how and why metabolic reprogramming occurs in tumor cells, and the mechanisms linking altered metabolism to tumorigenesis and metastasis will progressively support the development of new strategies to treat human cancer.Abstract:
Tumors reprogram pathways of nutrient acquisition and metabolism to meet the bioenergetic, biosynthetic, and redox demands of malignant cells. These reprogrammed activities are now recognized as hallmarks of cancer, and recent work has uncovered remarkable flexibility in the specific pathways activated by tumor cells to support these key functions. In this perspective, we provide a conceptual framework to understand how and why metabolic reprogramming occurs in tumor cells, and the mechanisms linking altered metabolism to tumorigenesis and metastasis. Understanding these concepts will progressively support the development of new strategies to treat human cancer.read more
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Dependence On Glycolysis Sensitizes BRAF-mutated Melanomas For Increased Response To Targeted BRAF Inhibition.
Keisha N. Hardeman,Chengwei Peng,B. Bishal Paudel,Christian T. Meyer,Thong Luong,Darren R. Tyson,Jamey D. Young,Vito Quaranta,Joshua P. Fessel +8 more
TL;DR: The data suggest that forcing tumor glycolysis in melanoma using zalcitabine or other similar approaches may be an adjunct to increase the efficacy of targeted BRAF therapy.
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Reactive metabolite production is a targetable liability of glycolytic metabolism in lung cancer.
Alba Luengo,Keene L. Abbott,Shawn M. Davidson,Shawn M. Davidson,Aaron M. Hosios,Brandon Faubert,Sze Ham Chan,Elizaveta Freinkman,Lauren G. Zacharias,Thomas P. Mathews,Clary B. Clish,Ralph J. DeBerardinis,Caroline A. Lewis,Matthew G. Vander Heiden +13 more
TL;DR: Evidence is presented that lactoylglutathione, a by-product of methylglyoxal produced from increased glycolysis, is elevated in lung cancer in mouse models and humans, arguing reactive metabolite production can be a liability for cancers.
Journal ArticleDOI
Biological and metabolic effects of IACS-010759, an OxPhos inhibitor, on chronic lymphocytic leukemia cells.
Hima V. Vangapandu,Brandon Alston,Joshua Morse,Mary Ayres,William G. Wierda,Michael J. Keating,Joseph R. Marszalek,Varsha Gandhi +7 more
TL;DR: It is suggested that CLL cells adapt to use a different metabolic pathway when OxPhos is inhibited and that targeting both Ox Phos and glycolysis pathways is necessary for biological effect.
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miR-450a Acts as a Tumor Suppressor in Ovarian Cancer by Regulating Energy Metabolism.
Bruna Rodrigues Muys,Josane F. Sousa,Jessica Rodrigues Plaça,Jessica Rodrigues Plaça,Luiza Ferreira de Araújo,Aishe A. Sarshad,Dimitrios G. Anastasakis,Xiantao Wang,Xiaoling Li,Greice Andreotti de Molfetta,Greice Andreotti de Molfetta,Anelisa Ramão,Anelisa Ramão,Ashish Lal,Daniel Onofre Vidal,Markus Hafner,Wilson A. Silva,Wilson A. Silva +17 more
TL;DR: It is proposed that miR-450a acts as a tumor suppressor in ovarian cancer cells by modulating targets associated with glutaminolysis, which leads to decreased production of lipids, amino acids, and nucleic acids as well as inhibition of signaling pathways associated with EMT.
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Mitochondrial VDAC1 Silencing Leads to Metabolic Rewiring and the Reprogramming of Tumour Cells into Advanced Differentiated States.
TL;DR: It is demonstrated that silencing VDAC1 expression using human-specific siRNA (si-hVDAC1) inhibited cancer cell growth, both in vitro and in mouse xenograft models of human glioblastoma, suggesting VDac1 to be an innovative and markedly potent therapeutic target.
References
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Journal ArticleDOI
Hallmarks of cancer: the next generation.
TL;DR: Recognition of the widespread applicability of these concepts will increasingly affect the development of new means to treat human cancer.
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How mitochondria produce reactive oxygen species.
TL;DR: The description outlined here facilitates the understanding of factors that favour mitochondrial ROS production and develops better methods to measure mitochondrial O2•− and H2O2 formation in vivo, as uncertainty about these values hampers studies on the role of mitochondrial ROS in pathological oxidative damage and redox signalling.
mTOR Signaling in Growth Control and Disease
TL;DR: The mechanistic target of rapamycin (mTOR) signaling pathway senses and integrates a variety of environmental cues to regulate organismal growth and homeostasis as mentioned in this paper, and is implicated in an increasing number of pathological conditions, including cancer, obesity, type 2 diabetes, and neurodegeneration.