Ruiz-Perez 2015 J Biol Chem: Difference between revisions
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|title=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 [Epub ahead of print]. | |title=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 [Epub ahead of print]. | ||
|authors=Ruiz-Perez MV, Medina MA, Urdiales JL, Keinaenen TA, Sanchez-Jimenez F | |authors=Ruiz-Perez MV, Medina MA, Urdiales JL, Keinaenen TA, Sanchez-Jimenez F | ||
|year=2015 | |year=2015 | ||
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|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. | |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 | |keywords=Cancer metabolism, Neuroblastoma, N-Myc, Polyamines, Glycolysis | ||
|mipnetlab=ES Malaga Medina MA | |||
}} | }} | ||
{{Labeling | {{Labeling |
Revision as of 09:49, 3 March 2015
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 [Epub ahead of print]. |
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
• O2k-Network Lab: ES Malaga Medina MA
Labels: MiParea: Respiration
Pathology: Cancer
Organism: Human Tissue;cell: Nervous system Preparation: Intact cells
Coupling state: LEAK, ROUTINE, OXPHOS, ETS"ETS" is not in the list (LEAK, ROUTINE, OXPHOS, ET) of allowed values for the "Coupling states" property.
HRR: Oxygraph-2k
Labels, [Epub ahead of print]