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Open AccessJournal ArticleDOI

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.

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Advances into understanding metabolites as signaling molecules in cancer progression

TL;DR: Recent advances in metabolic signaling through post-translational modification during cancer progression are reviewed to provide a framework for understanding signaling roles of metabolites in the context of cancer biology and illuminate areas for future investigation.
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Fluorescent probes for imaging bioactive species in subcellular organelles.

TL;DR: Luminescent molecular probes and nanoscale materials have become important tools in biosensing and bioimaging applications because of their high sensitivity, fast response, specificity, and methodological simplicity as discussed by the authors.
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Dysregulated FOXM1 Signaling in the regulation of cancer stem cells.

TL;DR: In this paper , a review compiles the large body of literature that has accumulated in recent years that provides evidence for the mechanisms by which FOXM1 expression promotes stemness in glioblastoma, breast, colon, ovarian, lung, hepatic, and pancreatic carcinomas.
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Remodeling of mitochondrial morphology and function: an emerging hallmark of cellular reprogramming.

TL;DR: This review of recent studies suggest an emerging landscape in which mitochondrial morphology and function have an active role in maintaining and regulating changes in cell identity, and recognition of the widespread applicability of these concepts will increase understanding of the mitochondrial mechanisms involved in cell Identity, cell fate and disease.
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Metabolic reprogramming sustains cancer cell survival following extracellular matrix detachment.

TL;DR: It is reported that cancer cells prioritize glutamine-derived tricarboxylic acid cycle energy metabolism over glycolysis to sustain anchorage-independent survival and is supported mainly by glutaminolysis via the AMPK-Nrf2 signal axis.
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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On the origin of cancer cells.

Origin of cancer cells

Otto Warburg
Journal ArticleDOI

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.
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