Difference between revisions of "Peruzzo 2016 Cell Cycle"
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{{Publication | {{Publication | ||
|title=Peruzzo P, Comelli M, Di Giorgio E, Franforte E, Mavelli I, Brancolini C (2016) Transformation by different oncogenes relies on specific metabolic adaptations. Cell Cycle 15:2656-68. | |title=Peruzzo P, Comelli M, Di Giorgio E, Franforte E, Mavelli I, Brancolini C (2016) Transformation by different oncogenes relies on specific metabolic adaptations. Cell Cycle 15:2656-68. | ||
|info=[ | |info=[http://www.ncbi.nlm.nih.gov/pubmed/27485932 PMID: 27485932] | ||
|authors=Peruzzo P, Comelli M, Di Giorgio E, Franforte E, Mavelli I, Brancolini C | |authors=Peruzzo P, Comelli M, Di Giorgio E, Franforte E, Mavelli I, Brancolini C | ||
|year=2016 | |year=2016 | ||
|journal=Cell Cycle | |journal=Cell Cycle | ||
|abstract=Metabolic adaptations are emerging as common traits of cancer cells and tumor progression. ''In vitro'' transformation of NIH 3T3 cells allows the analysis of the metabolic changes triggered by a single oncogene. In this work, we have compared the metabolic changes induced by H-RAS and by the nuclear resident mutant of histone deacetylase 4 (HDAC4). RAS-transformed cells exhibit a dominant aerobic glycolytic phenotype characterized by up-regulation of glycolytic enzymes, reduced oxygen consumption and a defect in complex I activity. In this model of transformation, glycolysis is strictly required for sustaining the ATP levels and the robust cellular proliferation. By contrast, in HDAC4/TM transformed cells, glycolysis is only modestly up-regulated, lactate secretion is not augmented and, instead, mitochondrial oxygen consumption is increased. Our results demonstrate that cellular transformation can be accomplished through different metabolic adaptations and HDAC4/TM cells can represent a useful model to investigate oncogene-driven metabolic changes besides the Warburg effect. | |abstract=Metabolic adaptations are emerging as common traits of cancer cells and tumor progression. ''In vitro'' transformation of NIH 3T3 cells allows the analysis of the metabolic changes triggered by a single oncogene. In this work, we have compared the metabolic changes induced by H-RAS and by the nuclear resident mutant of histone deacetylase 4 (HDAC4). RAS-transformed cells exhibit a dominant aerobic glycolytic phenotype characterized by up-regulation of glycolytic enzymes, reduced oxygen consumption and a defect in complex I activity. In this model of transformation, glycolysis is strictly required for sustaining the ATP levels and the robust cellular proliferation. By contrast, in HDAC4/TM transformed cells, glycolysis is only modestly up-regulated, lactate secretion is not augmented and, instead, mitochondrial oxygen consumption is increased. Our results demonstrate that cellular transformation can be accomplished through different metabolic adaptations and HDAC4/TM cells can represent a useful model to investigate oncogene-driven metabolic changes besides the Warburg effect. | ||
|keywords=CLN3, CPT1A, ENO2, GLA, Glycolysis, HDAC4, HDAC5, HDAC7, HDAC9, HK2, MEF2A, MEF2B, MEF2C, MEF2D, NSDHL, OXPHOS, PGK1, PKM2, RHOB, Warburg, class IIa, Mitochondria | |keywords=CLN3, CPT1A, ENO2, GLA, Glycolysis, HDAC4, HDAC5, HDAC7, HDAC9, HK2, MEF2A, MEF2B, MEF2C, MEF2D, NSDHL, OXPHOS, PGK1, PKM2, RHOB, Warburg, class IIa, Mitochondria, NIH 3T3 cells | ||
|mipnetlab=IT Udine Grassi B | |mipnetlab=IT Udine Grassi B, IT Udine Mavelli I | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
|area=Respiration, nDNA;cell genetics | |area=Respiration, nDNA;cell genetics, Genetic knockout;overexpression | ||
|diseases=Cancer | |||
|organism=Mouse | |organism=Mouse | ||
|tissues=Fibroblast | |||
|preparations=Intact cells | |preparations=Intact cells | ||
|couplingstates=LEAK, ROUTINE, ET | |||
|couplingstates=LEAK, ROUTINE, | |pathways=ROX | ||
| | |||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|additional= | |additional=2016-09 | ||
}} | }} | ||
Latest revision as of 13:59, 27 March 2018
| Peruzzo P, Comelli M, Di Giorgio E, Franforte E, Mavelli I, Brancolini C (2016) Transformation by different oncogenes relies on specific metabolic adaptations. Cell Cycle 15:2656-68. |
Peruzzo P, Comelli M, Di Giorgio E, Franforte E, Mavelli I, Brancolini C (2016) Cell Cycle
Abstract: Metabolic adaptations are emerging as common traits of cancer cells and tumor progression. In vitro transformation of NIH 3T3 cells allows the analysis of the metabolic changes triggered by a single oncogene. In this work, we have compared the metabolic changes induced by H-RAS and by the nuclear resident mutant of histone deacetylase 4 (HDAC4). RAS-transformed cells exhibit a dominant aerobic glycolytic phenotype characterized by up-regulation of glycolytic enzymes, reduced oxygen consumption and a defect in complex I activity. In this model of transformation, glycolysis is strictly required for sustaining the ATP levels and the robust cellular proliferation. By contrast, in HDAC4/TM transformed cells, glycolysis is only modestly up-regulated, lactate secretion is not augmented and, instead, mitochondrial oxygen consumption is increased. Our results demonstrate that cellular transformation can be accomplished through different metabolic adaptations and HDAC4/TM cells can represent a useful model to investigate oncogene-driven metabolic changes besides the Warburg effect. • Keywords: CLN3, CPT1A, ENO2, GLA, Glycolysis, HDAC4, HDAC5, HDAC7, HDAC9, HK2, MEF2A, MEF2B, MEF2C, MEF2D, NSDHL, OXPHOS, PGK1, PKM2, RHOB, Warburg, class IIa, Mitochondria, NIH 3T3 cells
• O2k-Network Lab: IT Udine Grassi B, IT Udine Mavelli I
Labels: MiParea: Respiration, nDNA;cell genetics, Genetic knockout;overexpression
Pathology: Cancer
Organism: Mouse Tissue;cell: Fibroblast Preparation: Intact cells
Coupling state: LEAK, ROUTINE, ET
Pathway: ROX
HRR: Oxygraph-2k
2016-09
