Peruzzo 2016 Cell Cycle

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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.

» PMID: 27485932

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