Targeting Cancer Metabolism - Revisiting the Warburg Effects

Tran, Quangdon; Lee, Hyunji; Park, Jisoo; Kim, Seon‐Hwan; Park, Jongsun

doi:10.5487/tr.2016.32.3.177

Cited by 96 publications

(89 citation statements)

References 170 publications

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“…In addition to surviving the hypoxic environment within a tumor, cancer cells predominantly use glycolysis both in aerobic and hypoxic environments (Vander Heiden et al, 2009, Tran et al, 2016). Altered isoforms and abnormal expression of glycolytic enzymes have been proposed as ways to achieve higher rates of glycolysis observed in cancer cells (Atsumi et al, 2002; Bustamante et al, 1981; Cairns et al, 2011; Christofk et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Glycolytic Enzymes Coalesce in G Bodies under Hypoxic Stress

et al. 2017

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SUMMARY Glycolysis is upregulated under conditions such as hypoxia and high energy demand to promote cell proliferation, although the mechanism remains poorly understood. We find that hypoxia in Saccharomyces cerevisiae induces concentration of glycolytic enzymes, including the Pfk2p subunit of the rate-limiting phosphofructokinase, into a single, non-membrane-bound granule termed the “glycolytic body” or “G body”. A yeast kinome screen identifies the yeast ortholog of AMP-activated protein kinase, Snf1p, as necessary for G body formation. Many G body components identified by proteomics are required for G body integrity. Cells incapable of forming G bodies in hypoxia display abnormal cell division and produce inviable daughter cells. Conversely, cells with G bodies show increased glucose consumption and decreased levels of glycolytic intermediates. Importantly, G bodies form in human hepatocarcinoma cells in hypoxia. Together, our results suggest that G body formation is a conserved, adaptive response to increase glycolytic output during hypoxia or tumorigenesis.

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Section: Introductionmentioning

confidence: 99%

Glycolytic Enzymes Coalesce in G Bodies under Hypoxic Stress

et al. 2017

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“…Targeting the metabolic differences between cancer and normal cells holds promise as a novel anti-cancer strategy [77]. Cancer cells usually use high level of ATP for their enhanced glycolytic metabolism (Warburg effect, [78]). Distinct UNBS1450mediated in vitro growth inhibitory effects between normal and cancer cells seemed to be correlated with a lower ATP level in cancer than in normal cells [57].…”

Section: Discussionmentioning

confidence: 99%

Characterisation of palytoxin from an undescribed Palythoa (Anthozoa: Zoantharia: Sphenopidae) with significant in vitro cytotoxic effects on cancer cells at picomolar doses

Sawelew

Gault²,

Nuccio

et al. 2018

Preprint

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Palytoxin (PlTX), a large polyhydroxylated compound, is among the most potent non-peptide toxin in marine organisms known so far. The literature emphasizes the sodium/potassium pump (NaK) as the privileged target for PlTX when exerting its toxic effects. In this study, we focused on an undescribed species (Palythoa sp. Pc001), a coral species belonging to the genus Palythoa routinely cultivated in aquariums. We demonstrated that this species contains one of the highest yields of pure PlTX production ever found, 2.22 ± 0.41 mg PlTX per gram of wet Palythoa. Using molecular data combined with external morphology, we identified Palythoa sp. Pc001 as the sister species to Palythoa aff. clavata. Further, the clade of a symbiotic Symbiodinium sp. was characterised by DNA barcoding and pigment content. 2

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“…As the study found out the protein rather form complex with the anti-apoptotic Bcl-2 protein myeloid cell leukemia-1 (Mcl-1) and stimulates improved glucose metabolism and enhances metabolism via the PPP, favoring synthesis ribose sugar and NADPH. Furthermore, subsequent studies showed that over expression of NOXA in tumor cells, and over activity of CDK5 to promote tumor growth and survival, specifically in thyroid and neuroendocrine tumors [46,47].…”

Section: Bcl-2 Proteinsmentioning

confidence: 99%

“…In addition to activation of oncogenes and loss of tumor suppressor pathways, mutations in key metabolic enzymes as well as preferential expression of specific isoforms of metabolic enzymes can provide cancer cells a mechanism to select for metabolic alterations during tumorigenesis [3,8,48].…”

Section: Metabolic Enzymesmentioning

confidence: 99%

Drivers of Glucose and Glutamine Metabolism Reprogramming in Tumor Cells and Their Potential as Target for Cancer

Mekuria¹,

Abdi²

2018

J Tumor Res

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Malignant cells undergo a metabolic transformation to satisfy the demands of growth and proliferation. This metabolic reprogramming has been considered as an emerging hallmark of cancer. It is well established that most normal cells get energy first via glycolysis in the cytosol that is followed by mitochondrial oxidative phosphorylation (OXPHO) under aerobic conditions but when oxygen is scarce, glycolysis rather than OXPHO for energy supply. However, cancer cells prefer to perform glycolysis in the cytosol even in the presence of oxygen, a phenomenon first observed by Otto Warburg and now famously known as ''Warburg effect'' or ''aerobic glycolysis''. Such reprogramming of glucose metabolism has been validated within many tumors, and increased glycolysis facilitates biosynthesis of biomass (e.g., nucleotides, amino acids and lipids) by providing glycolytic intermediates as raw material. Besides the dysregulation of glucose metabolism, metabolic reprogramming in cancer cells has been characterized by aberrant lipid metabolism, amino acids metabolism, mitochondrial biogenesis, and other bioenergetics metabolic pathways. However, the two noticeable characteristics of tumor cell metabolism are the Warburg effect and glutaminolysis, which, respectively, demonstrate the dependence of tumor cells on glucose and glutamine. Investigation on these metabolic changes would uncover fundamental molecular events of malignancy and help to find better ways to diagnose and treat cancer. This review aimed at appraising recent findings related to the drivers of glucose and glutamine metabolism reprogramming, their crosstalk in cancer cells, and their potential in cancer therapy. Underlining mechanismsThe fundamental mechanisms that lead to change in cancer cell metabolism continue to be clarified, but, existing literatures pointed out that alterations in numerous signaling pathways and altered expression and mutation of metabolic enzymes are central in mediating the unusual metabolic behavior of cancer cells [16][17][18].

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Targeting Cancer Metabolism - Revisiting the Warburg Effects

Cited by 96 publications

References 170 publications

Glycolytic Enzymes Coalesce in G Bodies under Hypoxic Stress

Glycolytic Enzymes Coalesce in G Bodies under Hypoxic Stress

Characterisation of palytoxin from an undescribed Palythoa (Anthozoa: Zoantharia: Sphenopidae) with significant in vitro cytotoxic effects on cancer cells at picomolar doses

Drivers of Glucose and Glutamine Metabolism Reprogramming in Tumor Cells and Their Potential as Target for Cancer

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