Elucidating the Metabolic Plasticity of Cancer: Mitochondrial Reprogramming and Hybrid Metabolic States

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dc.citation.articleNumber21en_US
dc.citation.issueNumber3en_US
dc.citation.journalTitleCellsen_US
dc.citation.volumeNumber7en_US
dc.contributor.authorJia, Dongyaen_US
dc.contributor.authorPark, Jun Hyoungen_US
dc.contributor.authorJung, Kwang Hwaen_US
dc.contributor.authorLevine, Herberten_US
dc.contributor.authorKaipparettu, Benny Abrahamen_US
dc.date.accessioned2018-07-16T17:48:56Zen_US
dc.date.available2018-07-16T17:48:56Zen_US
dc.date.issued2018en_US
dc.description.abstractAerobic glycolysis, also referred to as the Warburg effect, has been regarded as the dominant metabolic phenotype in cancer cells for a long time. More recently, it has been shown that mitochondria in most tumors are not defective in their ability to carry out oxidative phosphorylation (OXPHOS). Instead, in highly aggressive cancer cells, mitochondrial energy pathways are reprogrammed to meet the challenges of high energy demand, better utilization of available fuels and macromolecular synthesis for rapid cell division and migration. Mitochondrial energy reprogramming is also involved in the regulation of oncogenic pathways via mitochondria-to-nucleus retrograde signaling and post-translational modification of oncoproteins. In addition, neoplastic mitochondria can engage in crosstalk with the tumor microenvironment. For example, signals from cancer-associated fibroblasts can drive tumor mitochondria to utilize OXPHOS, a process known as the reverse Warburg effect. Emerging evidence shows that cancer cells can acquire a hybrid glycolysis/OXPHOS phenotype in which both glycolysis and OXPHOS can be utilized for energy production and biomass synthesis. The hybrid glycolysis/OXPHOS phenotype facilitates metabolic plasticity of cancer cells and may be specifically associated with metastasis and therapy-resistance. Moreover, cancer cells can switch their metabolism phenotypes in response to external stimuli for better survival. Taking into account the metabolic heterogeneity and plasticity of cancer cells, therapies targeting cancer metabolic dependency in principle can be made more effective.en_US
dc.identifier.citationJia, Dongya, Park, Jun Hyoung, Jung, Kwang Hwa, et al.. "Elucidating the Metabolic Plasticity of Cancer: Mitochondrial Reprogramming and Hybrid Metabolic States." <i>Cells,</i> 7, no. 3 (2018) MDPI: https://doi.org/10.3390/cells7030021.en_US
dc.identifier.doihttps://doi.org/10.3390/cells7030021en_US
dc.identifier.urihttps://hdl.handle.net/1911/102423en_US
dc.language.isoengen_US
dc.publisherMDPIen_US
dc.rightsThis article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).en_US
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/en_US
dc.subject.keywordcancer metabolismen_US
dc.subject.keywordWarburg effecten_US
dc.subject.keywordoxidative phosphorylationen_US
dc.subject.keywordOXPHOSen_US
dc.subject.keywordmitochondrial respirationen_US
dc.subject.keywordhybrid metabolic phenotypeen_US
dc.subject.keywordmetabolic plasticityen_US
dc.subject.keywordtumorigenesisen_US
dc.subject.keywordmetastasisen_US
dc.subject.keywordEMTen_US
dc.subject.keywordstemnessen_US
dc.titleElucidating the Metabolic Plasticity of Cancer: Mitochondrial Reprogramming and Hybrid Metabolic Statesen_US
dc.typeJournal articleen_US
dc.type.dcmiTexten_US
dc.type.publicationpublisher versionen_US
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