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Ruiz-Perez 2015 J Biol Chem

From Bioblast
Publications in the MiPMap
Ruiz-Pérez MV, Medina MÁ, Urdiales JL, Keinänen TA, Sánchez-Jiménez F (2015) Polyamine metabolism is sensitive to glycolysis inhibition in human neuroblastoma cells. J Biol Chem 290:6106-19.

» PMID:25593318

Ruiz-Perez MV, Medina MA, Urdiales JL, Keinaenen TA, Sanchez-Jimenez F (2015) J Biol Chem

Abstract: Polyamines are essential for cell proliferation, and their levels are elevated in many human tumours. The oncogene n-myc is known to potentiate polyamine metabolism. Neuroblastoma, the most frequent extra-cranial solid tumour in children, harbours the amplification of n-myc oncogene in 25% of the cases, and it is associated with treatment failure and poor prognosis. We evaluated several metabolic features of the human neuroblastoma cell lines Kelly, IMR-32 and SK-N-SH. We further investigated the effects of glycolysis impairment in polyamine metabolism in these cell lines. A previously unknown linkage between glycolysis impairment and polyamine reduction is unveiled. We show that glycolysis inhibition is able to trigger signalling events leading to the reduction of N-Myc protein levels and a subsequent decrease of both ornithine decarboxylase expression and polyamine levels, accompanied by cell cycle blockade preceding cell death. New anti-tumour strategies could take advantage of the direct relationship between glucose deprivation and PA metabolism impairment leading to cell death and its apparent dependence on n-myc. Combined therapies targeting glucose metabolism and PA synthesis could be effective in the treatment of n-myc-expressing tumours. Keywords: Cancer metabolism, Neuroblastoma, N-Myc, Polyamines, Glycolysis, Human neuroblastoma cells Kelly, IMR-32, SK-N-SH

O2k-Network Lab: ES Malaga Medina MA


Labels: MiParea: Respiration  Pathology: Cancer 

Organism: Human  Tissue;cell: Nervous system, Other cell lines, Neuroblastoma  Preparation: Intact cells 


Coupling state: LEAK, ROUTINE, ET  Pathway: ROX  HRR: Oxygraph-2k 

Spermidine