Erratum: Cancer metabolism: a therapeutic perspective

Martinez‐Outschoorn, Ubaldo; Peiris-Pagès, Maria; Pestell, Richard G.; Sotgia, Federica; Lisanti, Michael P.

doi:10.1038/nrclinonc.2017.1

Cited by 173 publications

(92 citation statements)

References 1 publication

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“…Hypoxia is recognized as a fundamentally important feature of solid tumors and is at the heart of cancer hallmarks . Under hypoxia, metabolic pathways of cancer cells may therefore be rewired in such a way that balances biosynthetic processes with rapid and large amounts of ATP production to support cell proliferation, a phenomenon referred to as aerobic glycolysis or the “Warburg effect” that is uniquely observed in primary and metastatic tumors . The high rate of glycolysis is associated with excessive generation of lactic acid, which leads to the upregulation of monocarboxylate transporters (MCTs), predominantly MCT4, for efflux of lactate/H + to maintain a stable intracellular pH and induce an acidic tumor microenvironment.…”

Section: Methodsmentioning

confidence: 99%

Engineering Multifunctional RNAi Nanomedicine To Concurrently Target Cancer Hallmarks for Combinatorial Therapy

Liu

Tong

et al. 2018

Angewandte Chemie

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Cancer hallmarks allowt he complexity and heterogeneity of tumor biology to be better understood, leading to the discovery of various promising targets for cancer therapy. An amorphous iron oxide nanoparticle (NP)-based RNAi strategy is developed to co-target two cancer hallmarks.T he NP technology can modulate the glycolysis pathway by silencing MCT4 to induce tumor cell acidosis,a nd concurrently exacerbate oxidative stress in tumor cells via the Fenton-like reaction. This strategy has the following features for systemic siRNAd elivery:1 )siRNAe ncapsulation within NPs for improving systemic stability;2 )effective endosomal escape through osmotic pressure and/or endosomal membrane oxidation;3 )small sizef or enhancing tumor tissue penetration; and 4) triple functions (RNAi, Fenton-like reaction, and MRI) for combinatorial therapya nd in vivo tracking.Scheme 1. Illustration of A) the formulation and B) multiple functions of AIO RNAi NPs.

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Section: Methodsmentioning

confidence: 99%

Engineering Multifunctional RNAi Nanomedicine To Concurrently Target Cancer Hallmarks for Combinatorial Therapy

Liu

Tong

et al. 2018

Angewandte Chemie

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“…Reprogrammed energy metabolism is emerged as a hallmark of cancer cells [1]. Different from normal cells, cancer cells preferentially utilize glycolysis instead of oxidative phosphorylation to produce energy even in the presence of sufficient oxygen, a phenomenon called aerobic glycolysis, also known as the Warburg effect [2,3]. In addition, cancer cells are addicted to the amino acid glutamine to fuel anabolic processes [4].…”

Section: Introductionmentioning

confidence: 99%

GFAT1/HBP/O-GlcNAcylation Axis Regulatesβ-Catenin Activity to Promote Pancreatic Cancer Aggressiveness

Jia

et al. 2020

BioMed Research International

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Reprogrammed glucose and glutamine metabolism are essential for tumor initiation and development. As a branch of glucose and metabolism, the hexosamine biosynthesis pathway (HBP) generates uridine diphosphate N-acetylglucosamine (UDP-GlcNAc) and contributes to the O-GlcNAcylation process. However, the spectrum of HBP-dependent tumors and the mechanisms by which the HBP promotes tumor aggressiveness remain areas of active investigation. In this study, we analyzed the activity of the HBP and its prognostic value across 33 types of human cancers. Increased HBP activity was observed in pancreatic ductal adenocarcinoma (PDAC), and higher HBP activity predicted a poor prognosis in PDAC patients. Genetic silencing or pharmacological inhibition of the first and rate-limiting enzyme of the HBP, glutamine:fructose-6-phosphate amidotransferase 1 (GFAT1), inhibited PDAC cell proliferation, invasive capacity, and triggered cell apoptosis. Notably, these effects can be restored by addition of UDP-GlcNAc. Moreover, similar antitumor effects were noticed by pharmacological inhibition of GFAT1 with 6-diazo-5-oxo-lnorleucine (DON) or Azaserine. PDAC is maintained by oncogenic Wnt/β-catenin transcriptional activity. Our data showed that GFAT1 can regulate β-catenin expression via modulation of the O-GlcNAcylation process. TOP/FOP-Flash and real-time qPCR analysis showed that GFAT1 knockdown inhibited β-catenin activity and the transcription of its downstream target genes CCND1 and MYC. Ectopic expression of a stabilized form of β-catenin restored the suppressive roles of GFAT1 knockdown on PDAC cell proliferation and invasion. Collectively, our findings indicate that higher GFAT1/HBP/O-GlcNAcylation exhibits tumor-promoting roles by maintaining β-catenin activity in PDAC.

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“…Most recently, we developed a novel strategy to measure 2‐NBDG and TMRE simultaneously using intravital microscopy in a window chamber tumor model . To translate simultaneous quantification of key metabolic endpoints to solid tumor models that are often used for therapeutic studies , we have also demonstrated the capability of a quantitative spectroscopy system to quantify 2‐NBDG and TMRE fluorescence along with key vascular parameters (SO 2 and [Hb]) on preclinical solid tumor model .…”

Section: Introductionmentioning

confidence: 99%

Simultaneous in vivo optical quantification of key metabolic and vascular endpoints reveals tumor metabolic diversity in murine breast tumor models

Zhu

Vincent

et al. 2019

Journal of Biophotonics

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Therapeutically exploiting vascular and metabolic endpoints becomes critical to translational cancer studies because altered vascularity and deregulated metabolism are two important cancer hallmarks. The metabolic and vascular phenotypes of three sibling breast tumor lines with different metastatic potential are investigated in vivo with a newly developed quantitative spectroscopy system. All tumor lines have different metabolic and vascular characteristics compared to normal tissues, and there are strong positive correlations between metabolic (glucose uptake and mitochondrial membrane potential) and vascular (oxygen saturations and hemoglobin concentrations) parameters for metastatic (4T1) tumors but not for micrometastatic (4T07) and nonmetastatic (67NR) tumors. A longitudinal study shows that both vascular and metabolic endpoints of 4T1 tumors increased up to a specific tumor size threshold beyond which these parameters decreased. The synchronous changes between metabolic and vascular parameters, along with the strong positive correlations between these endpoints suggest that 4T1 tumors rely on strong oxidative phosphorylation in addition to glycolysis. This study illustrates the great potential of our optical technique to provide valuable dynamic information about the interplay between the metabolic and vascular status of tumors, with important implications for translational cancer investigations. K E Y W O R D Soptical spectroscopy, tumor metabolism, tumor metastasis, vascular microenvironmentInterest in metabolism and the vascular microenvironment continues to grow in a broad range of disciplines including neuroscience [1], cardiovascular biology [2] and the field of cancer research [3]. At the most basic level, lack of oxygen promotes glycolysis to allow biological systems to survive acute stress [4]. Under conditions of chronic stress, such as persistent hypoxia, biological cells can undergo long-term changes that allow their metabolism and supporting

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Erratum: Cancer metabolism: a therapeutic perspective

Cited by 173 publications

References 1 publication

Engineering Multifunctional RNAi Nanomedicine To Concurrently Target Cancer Hallmarks for Combinatorial Therapy

Engineering Multifunctional RNAi Nanomedicine To Concurrently Target Cancer Hallmarks for Combinatorial Therapy

GFAT1/HBP/O-GlcNAcylation Axis Regulatesβ-Catenin Activity to Promote Pancreatic Cancer Aggressiveness

Simultaneous in vivo optical quantification of key metabolic and vascular endpoints reveals tumor metabolic diversity in murine breast tumor models

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