Difference between revisions of "Ruiz-Perez 2015 J Biol Chem"
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{{Publication | {{Publication | ||
|title=Ruiz-PĂ©rez MV, Medina MĂ, Urdiales JL, KeinĂ€nen TA, SĂĄnchez-JimĂ©nez F (2015) Polyamine metabolism is sensitive to glycolysis inhibition in human neuroblastoma cells. J Biol Chem [ | |title=Ruiz-PĂ©rez MV, Medina MĂ, Urdiales JL, KeinĂ€nen TA, SĂĄnchez-JimĂ©nez F (2015) Polyamine metabolism is sensitive to glycolysis inhibition in human neuroblastoma cells. J Biol Chem 290:6106-19. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/25593318 PMID:25593318] | |||
|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 | ||
|journal=J Biol Chem | |journal=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. | |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, Human neuroblastoma cells Kelly, IMR-32, SK-N-SH | ||
|mipnetlab=ES Malaga Medina MA | |mipnetlab=ES Malaga Medina MA | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
|area=Respiration | |area=Respiration | ||
|diseases=Cancer | |||
|organism=Human | |organism=Human | ||
|tissues=Nervous system | |tissues=Nervous system, Other cell lines, Neuroblastoma | ||
|preparations=Intact cells | |preparations=Intact cells | ||
|couplingstates=LEAK, ROUTINE, ET | |||
|couplingstates=LEAK, ROUTINE, | |pathways=ROX | ||
| | |||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|additional= | |additional=Spermidine | ||
}} | }} | ||
Latest revision as of 00:09, 9 April 2023
| Ruiz-PĂ©rez MV, Medina MĂ, Urdiales JL, KeinĂ€nen TA, SĂĄnchez-JimĂ©nez F (2015) Polyamine metabolism is sensitive to glycolysis inhibition in human neuroblastoma cells. J Biol Chem 290:6106-19. |
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. âą Keywords: Cancer metabolism, Neuroblastoma, N-Myc, Polyamines, Glycolysis, Human neuroblastoma cells Kelly, IMR-32, SK-N-SH
âą 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
