Sodium Ascorbate induces apoptosis in neuroblastoma cell lines by interfering with iron uptake

Background Neuroblastoma (NB) is an extra-cranial solid tumour of childhood. In spite of the good clinical response to first-line therapy, complete eradication of NB cells is rarely achieved. Thus, new therapeutic strategies are needed to eradicate surviving NB cells and prevent relapse. Sodium asco...
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Autor*in:	Carosio, Roberta [verfasserIn] Zuccari, Guendalina Orienti, Isabella Mangraviti, Salvatore Montaldo, Paolo G

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2007

Schlagwörter:	Mitochondrial Membrane Potential Transferrin Receptor Neuroblastoma Cell Line Sodium Ascorbate Mitochondrial Transmembrane Potential

Anmerkung:	© Carosio et al; licensee BioMed Central Ltd. 2007

Übergeordnetes Werk:	Enthalten in: Molecular cancer - London : Biomed Central, 2002, 6(2007), 1 vom: 30. Aug.
Übergeordnetes Werk:	volume:6 ; year:2007 ; number:1 ; day:30 ; month:08

Links:	Volltext

DOI / URN:	10.1186/1476-4598-6-55

Katalog-ID:	SPR028880781

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520			\|a Background Neuroblastoma (NB) is an extra-cranial solid tumour of childhood. In spite of the good clinical response to first-line therapy, complete eradication of NB cells is rarely achieved. Thus, new therapeutic strategies are needed to eradicate surviving NB cells and prevent relapse. Sodium ascorbate has been recently reported to induce apoptosis of B16 melanoma cells through down-regulation of the transferrin receptor, CD71. Since NB and melanoma share the same embryologic neuroectodermal origin, we used different human NB cell lines to assess whether the same findings occurred. Results We could observe dose- and time-dependent induction of apoptosis in all NB cell lines. Sodium ascorbate decreased the expression of CD71 and caused cell death within 24 h. An increase in the global and specific caspase activity took place, as well as an early loss of the mitochondrial transmembrane potential. Moreover, intracellular iron was significantly decreased after exposure to sodium ascorbate. Apoptotic markers were reverted when the cells were pretreated with the iron donor ferric ammonium citrate (FAC), further confirming that iron depletion is responsible for the ascorbate-induced cell death in NB cells. Conclusion Sodium ascorbate is highly toxic to neuroblastoma cell lines and the specific mechanism of vitamin C-induced apoptosis is due to a perturbation of intracellular iron levels ensuing TfR-downregulation.
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allfields	10.1186/1476-4598-6-55 doi (DE-627)SPR028880781 (SPR)1476-4598-6-55-e DE-627 ger DE-627 rakwb eng Carosio, Roberta verfasserin aut Sodium Ascorbate induces apoptosis in neuroblastoma cell lines by interfering with iron uptake 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Carosio et al; licensee BioMed Central Ltd. 2007 Background Neuroblastoma (NB) is an extra-cranial solid tumour of childhood. In spite of the good clinical response to first-line therapy, complete eradication of NB cells is rarely achieved. Thus, new therapeutic strategies are needed to eradicate surviving NB cells and prevent relapse. Sodium ascorbate has been recently reported to induce apoptosis of B16 melanoma cells through down-regulation of the transferrin receptor, CD71. Since NB and melanoma share the same embryologic neuroectodermal origin, we used different human NB cell lines to assess whether the same findings occurred. Results We could observe dose- and time-dependent induction of apoptosis in all NB cell lines. Sodium ascorbate decreased the expression of CD71 and caused cell death within 24 h. An increase in the global and specific caspase activity took place, as well as an early loss of the mitochondrial transmembrane potential. Moreover, intracellular iron was significantly decreased after exposure to sodium ascorbate. Apoptotic markers were reverted when the cells were pretreated with the iron donor ferric ammonium citrate (FAC), further confirming that iron depletion is responsible for the ascorbate-induced cell death in NB cells. Conclusion Sodium ascorbate is highly toxic to neuroblastoma cell lines and the specific mechanism of vitamin C-induced apoptosis is due to a perturbation of intracellular iron levels ensuing TfR-downregulation. Mitochondrial Membrane Potential (dpeaa)DE-He213 Transferrin Receptor (dpeaa)DE-He213 Neuroblastoma Cell Line (dpeaa)DE-He213 Sodium Ascorbate (dpeaa)DE-He213 Mitochondrial Transmembrane Potential (dpeaa)DE-He213 Zuccari, Guendalina aut Orienti, Isabella aut Mangraviti, Salvatore aut Montaldo, Paolo G aut Enthalten in Molecular cancer London : Biomed Central, 2002 6(2007), 1 vom: 30. Aug. (DE-627)355987619 (DE-600)2091373-4 1476-4598 nnns volume:6 year:2007 number:1 day:30 month:08 https://dx.doi.org/10.1186/1476-4598-6-55 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 6 2007 1 30 08
spelling	10.1186/1476-4598-6-55 doi (DE-627)SPR028880781 (SPR)1476-4598-6-55-e DE-627 ger DE-627 rakwb eng Carosio, Roberta verfasserin aut Sodium Ascorbate induces apoptosis in neuroblastoma cell lines by interfering with iron uptake 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Carosio et al; licensee BioMed Central Ltd. 2007 Background Neuroblastoma (NB) is an extra-cranial solid tumour of childhood. In spite of the good clinical response to first-line therapy, complete eradication of NB cells is rarely achieved. Thus, new therapeutic strategies are needed to eradicate surviving NB cells and prevent relapse. Sodium ascorbate has been recently reported to induce apoptosis of B16 melanoma cells through down-regulation of the transferrin receptor, CD71. Since NB and melanoma share the same embryologic neuroectodermal origin, we used different human NB cell lines to assess whether the same findings occurred. Results We could observe dose- and time-dependent induction of apoptosis in all NB cell lines. Sodium ascorbate decreased the expression of CD71 and caused cell death within 24 h. An increase in the global and specific caspase activity took place, as well as an early loss of the mitochondrial transmembrane potential. Moreover, intracellular iron was significantly decreased after exposure to sodium ascorbate. Apoptotic markers were reverted when the cells were pretreated with the iron donor ferric ammonium citrate (FAC), further confirming that iron depletion is responsible for the ascorbate-induced cell death in NB cells. Conclusion Sodium ascorbate is highly toxic to neuroblastoma cell lines and the specific mechanism of vitamin C-induced apoptosis is due to a perturbation of intracellular iron levels ensuing TfR-downregulation. Mitochondrial Membrane Potential (dpeaa)DE-He213 Transferrin Receptor (dpeaa)DE-He213 Neuroblastoma Cell Line (dpeaa)DE-He213 Sodium Ascorbate (dpeaa)DE-He213 Mitochondrial Transmembrane Potential (dpeaa)DE-He213 Zuccari, Guendalina aut Orienti, Isabella aut Mangraviti, Salvatore aut Montaldo, Paolo G aut Enthalten in Molecular cancer London : Biomed Central, 2002 6(2007), 1 vom: 30. Aug. (DE-627)355987619 (DE-600)2091373-4 1476-4598 nnns volume:6 year:2007 number:1 day:30 month:08 https://dx.doi.org/10.1186/1476-4598-6-55 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 6 2007 1 30 08
allfields_unstemmed	10.1186/1476-4598-6-55 doi (DE-627)SPR028880781 (SPR)1476-4598-6-55-e DE-627 ger DE-627 rakwb eng Carosio, Roberta verfasserin aut Sodium Ascorbate induces apoptosis in neuroblastoma cell lines by interfering with iron uptake 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Carosio et al; licensee BioMed Central Ltd. 2007 Background Neuroblastoma (NB) is an extra-cranial solid tumour of childhood. In spite of the good clinical response to first-line therapy, complete eradication of NB cells is rarely achieved. Thus, new therapeutic strategies are needed to eradicate surviving NB cells and prevent relapse. Sodium ascorbate has been recently reported to induce apoptosis of B16 melanoma cells through down-regulation of the transferrin receptor, CD71. Since NB and melanoma share the same embryologic neuroectodermal origin, we used different human NB cell lines to assess whether the same findings occurred. Results We could observe dose- and time-dependent induction of apoptosis in all NB cell lines. Sodium ascorbate decreased the expression of CD71 and caused cell death within 24 h. An increase in the global and specific caspase activity took place, as well as an early loss of the mitochondrial transmembrane potential. Moreover, intracellular iron was significantly decreased after exposure to sodium ascorbate. Apoptotic markers were reverted when the cells were pretreated with the iron donor ferric ammonium citrate (FAC), further confirming that iron depletion is responsible for the ascorbate-induced cell death in NB cells. Conclusion Sodium ascorbate is highly toxic to neuroblastoma cell lines and the specific mechanism of vitamin C-induced apoptosis is due to a perturbation of intracellular iron levels ensuing TfR-downregulation. Mitochondrial Membrane Potential (dpeaa)DE-He213 Transferrin Receptor (dpeaa)DE-He213 Neuroblastoma Cell Line (dpeaa)DE-He213 Sodium Ascorbate (dpeaa)DE-He213 Mitochondrial Transmembrane Potential (dpeaa)DE-He213 Zuccari, Guendalina aut Orienti, Isabella aut Mangraviti, Salvatore aut Montaldo, Paolo G aut Enthalten in Molecular cancer London : Biomed Central, 2002 6(2007), 1 vom: 30. Aug. (DE-627)355987619 (DE-600)2091373-4 1476-4598 nnns volume:6 year:2007 number:1 day:30 month:08 https://dx.doi.org/10.1186/1476-4598-6-55 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 6 2007 1 30 08
allfieldsGer	10.1186/1476-4598-6-55 doi (DE-627)SPR028880781 (SPR)1476-4598-6-55-e DE-627 ger DE-627 rakwb eng Carosio, Roberta verfasserin aut Sodium Ascorbate induces apoptosis in neuroblastoma cell lines by interfering with iron uptake 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Carosio et al; licensee BioMed Central Ltd. 2007 Background Neuroblastoma (NB) is an extra-cranial solid tumour of childhood. In spite of the good clinical response to first-line therapy, complete eradication of NB cells is rarely achieved. Thus, new therapeutic strategies are needed to eradicate surviving NB cells and prevent relapse. Sodium ascorbate has been recently reported to induce apoptosis of B16 melanoma cells through down-regulation of the transferrin receptor, CD71. Since NB and melanoma share the same embryologic neuroectodermal origin, we used different human NB cell lines to assess whether the same findings occurred. Results We could observe dose- and time-dependent induction of apoptosis in all NB cell lines. Sodium ascorbate decreased the expression of CD71 and caused cell death within 24 h. An increase in the global and specific caspase activity took place, as well as an early loss of the mitochondrial transmembrane potential. Moreover, intracellular iron was significantly decreased after exposure to sodium ascorbate. Apoptotic markers were reverted when the cells were pretreated with the iron donor ferric ammonium citrate (FAC), further confirming that iron depletion is responsible for the ascorbate-induced cell death in NB cells. Conclusion Sodium ascorbate is highly toxic to neuroblastoma cell lines and the specific mechanism of vitamin C-induced apoptosis is due to a perturbation of intracellular iron levels ensuing TfR-downregulation. Mitochondrial Membrane Potential (dpeaa)DE-He213 Transferrin Receptor (dpeaa)DE-He213 Neuroblastoma Cell Line (dpeaa)DE-He213 Sodium Ascorbate (dpeaa)DE-He213 Mitochondrial Transmembrane Potential (dpeaa)DE-He213 Zuccari, Guendalina aut Orienti, Isabella aut Mangraviti, Salvatore aut Montaldo, Paolo G aut Enthalten in Molecular cancer London : Biomed Central, 2002 6(2007), 1 vom: 30. Aug. (DE-627)355987619 (DE-600)2091373-4 1476-4598 nnns volume:6 year:2007 number:1 day:30 month:08 https://dx.doi.org/10.1186/1476-4598-6-55 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 6 2007 1 30 08
allfieldsSound	10.1186/1476-4598-6-55 doi (DE-627)SPR028880781 (SPR)1476-4598-6-55-e DE-627 ger DE-627 rakwb eng Carosio, Roberta verfasserin aut Sodium Ascorbate induces apoptosis in neuroblastoma cell lines by interfering with iron uptake 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Carosio et al; licensee BioMed Central Ltd. 2007 Background Neuroblastoma (NB) is an extra-cranial solid tumour of childhood. In spite of the good clinical response to first-line therapy, complete eradication of NB cells is rarely achieved. Thus, new therapeutic strategies are needed to eradicate surviving NB cells and prevent relapse. Sodium ascorbate has been recently reported to induce apoptosis of B16 melanoma cells through down-regulation of the transferrin receptor, CD71. Since NB and melanoma share the same embryologic neuroectodermal origin, we used different human NB cell lines to assess whether the same findings occurred. Results We could observe dose- and time-dependent induction of apoptosis in all NB cell lines. Sodium ascorbate decreased the expression of CD71 and caused cell death within 24 h. An increase in the global and specific caspase activity took place, as well as an early loss of the mitochondrial transmembrane potential. Moreover, intracellular iron was significantly decreased after exposure to sodium ascorbate. Apoptotic markers were reverted when the cells were pretreated with the iron donor ferric ammonium citrate (FAC), further confirming that iron depletion is responsible for the ascorbate-induced cell death in NB cells. Conclusion Sodium ascorbate is highly toxic to neuroblastoma cell lines and the specific mechanism of vitamin C-induced apoptosis is due to a perturbation of intracellular iron levels ensuing TfR-downregulation. Mitochondrial Membrane Potential (dpeaa)DE-He213 Transferrin Receptor (dpeaa)DE-He213 Neuroblastoma Cell Line (dpeaa)DE-He213 Sodium Ascorbate (dpeaa)DE-He213 Mitochondrial Transmembrane Potential (dpeaa)DE-He213 Zuccari, Guendalina aut Orienti, Isabella aut Mangraviti, Salvatore aut Montaldo, Paolo G aut Enthalten in Molecular cancer London : Biomed Central, 2002 6(2007), 1 vom: 30. Aug. (DE-627)355987619 (DE-600)2091373-4 1476-4598 nnns volume:6 year:2007 number:1 day:30 month:08 https://dx.doi.org/10.1186/1476-4598-6-55 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 6 2007 1 30 08
language	English
source	Enthalten in Molecular cancer 6(2007), 1 vom: 30. Aug. volume:6 year:2007 number:1 day:30 month:08
sourceStr	Enthalten in Molecular cancer 6(2007), 1 vom: 30. Aug. volume:6 year:2007 number:1 day:30 month:08
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Mitochondrial Membrane Potential Transferrin Receptor Neuroblastoma Cell Line Sodium Ascorbate Mitochondrial Transmembrane Potential
isfreeaccess_bool	true
container_title	Molecular cancer
authorswithroles_txt_mv	Carosio, Roberta @@aut@@ Zuccari, Guendalina @@aut@@ Orienti, Isabella @@aut@@ Mangraviti, Salvatore @@aut@@ Montaldo, Paolo G @@aut@@
publishDateDaySort_date	2007-08-30T00:00:00Z
hierarchy_top_id	355987619
id	SPR028880781
language_de	englisch
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In spite of the good clinical response to first-line therapy, complete eradication of NB cells is rarely achieved. Thus, new therapeutic strategies are needed to eradicate surviving NB cells and prevent relapse. Sodium ascorbate has been recently reported to induce apoptosis of B16 melanoma cells through down-regulation of the transferrin receptor, CD71. Since NB and melanoma share the same embryologic neuroectodermal origin, we used different human NB cell lines to assess whether the same findings occurred. Results We could observe dose- and time-dependent induction of apoptosis in all NB cell lines. Sodium ascorbate decreased the expression of CD71 and caused cell death within 24 h. An increase in the global and specific caspase activity took place, as well as an early loss of the mitochondrial transmembrane potential. Moreover, intracellular iron was significantly decreased after exposure to sodium ascorbate. 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author	Carosio, Roberta
spellingShingle	Carosio, Roberta misc Mitochondrial Membrane Potential misc Transferrin Receptor misc Neuroblastoma Cell Line misc Sodium Ascorbate misc Mitochondrial Transmembrane Potential Sodium Ascorbate induces apoptosis in neuroblastoma cell lines by interfering with iron uptake
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topic_title	Sodium Ascorbate induces apoptosis in neuroblastoma cell lines by interfering with iron uptake Mitochondrial Membrane Potential (dpeaa)DE-He213 Transferrin Receptor (dpeaa)DE-He213 Neuroblastoma Cell Line (dpeaa)DE-He213 Sodium Ascorbate (dpeaa)DE-He213 Mitochondrial Transmembrane Potential (dpeaa)DE-He213
topic	misc Mitochondrial Membrane Potential misc Transferrin Receptor misc Neuroblastoma Cell Line misc Sodium Ascorbate misc Mitochondrial Transmembrane Potential
topic_unstemmed	misc Mitochondrial Membrane Potential misc Transferrin Receptor misc Neuroblastoma Cell Line misc Sodium Ascorbate misc Mitochondrial Transmembrane Potential
topic_browse	misc Mitochondrial Membrane Potential misc Transferrin Receptor misc Neuroblastoma Cell Line misc Sodium Ascorbate misc Mitochondrial Transmembrane Potential
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title	Sodium Ascorbate induces apoptosis in neuroblastoma cell lines by interfering with iron uptake
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title_full	Sodium Ascorbate induces apoptosis in neuroblastoma cell lines by interfering with iron uptake
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author_browse	Carosio, Roberta Zuccari, Guendalina Orienti, Isabella Mangraviti, Salvatore Montaldo, Paolo G
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title_sort	sodium ascorbate induces apoptosis in neuroblastoma cell lines by interfering with iron uptake
title_auth	Sodium Ascorbate induces apoptosis in neuroblastoma cell lines by interfering with iron uptake
abstract	Background Neuroblastoma (NB) is an extra-cranial solid tumour of childhood. In spite of the good clinical response to first-line therapy, complete eradication of NB cells is rarely achieved. Thus, new therapeutic strategies are needed to eradicate surviving NB cells and prevent relapse. Sodium ascorbate has been recently reported to induce apoptosis of B16 melanoma cells through down-regulation of the transferrin receptor, CD71. Since NB and melanoma share the same embryologic neuroectodermal origin, we used different human NB cell lines to assess whether the same findings occurred. Results We could observe dose- and time-dependent induction of apoptosis in all NB cell lines. Sodium ascorbate decreased the expression of CD71 and caused cell death within 24 h. An increase in the global and specific caspase activity took place, as well as an early loss of the mitochondrial transmembrane potential. Moreover, intracellular iron was significantly decreased after exposure to sodium ascorbate. Apoptotic markers were reverted when the cells were pretreated with the iron donor ferric ammonium citrate (FAC), further confirming that iron depletion is responsible for the ascorbate-induced cell death in NB cells. Conclusion Sodium ascorbate is highly toxic to neuroblastoma cell lines and the specific mechanism of vitamin C-induced apoptosis is due to a perturbation of intracellular iron levels ensuing TfR-downregulation. © Carosio et al; licensee BioMed Central Ltd. 2007
abstractGer	Background Neuroblastoma (NB) is an extra-cranial solid tumour of childhood. In spite of the good clinical response to first-line therapy, complete eradication of NB cells is rarely achieved. Thus, new therapeutic strategies are needed to eradicate surviving NB cells and prevent relapse. Sodium ascorbate has been recently reported to induce apoptosis of B16 melanoma cells through down-regulation of the transferrin receptor, CD71. Since NB and melanoma share the same embryologic neuroectodermal origin, we used different human NB cell lines to assess whether the same findings occurred. Results We could observe dose- and time-dependent induction of apoptosis in all NB cell lines. Sodium ascorbate decreased the expression of CD71 and caused cell death within 24 h. An increase in the global and specific caspase activity took place, as well as an early loss of the mitochondrial transmembrane potential. Moreover, intracellular iron was significantly decreased after exposure to sodium ascorbate. Apoptotic markers were reverted when the cells were pretreated with the iron donor ferric ammonium citrate (FAC), further confirming that iron depletion is responsible for the ascorbate-induced cell death in NB cells. Conclusion Sodium ascorbate is highly toxic to neuroblastoma cell lines and the specific mechanism of vitamin C-induced apoptosis is due to a perturbation of intracellular iron levels ensuing TfR-downregulation. © Carosio et al; licensee BioMed Central Ltd. 2007
abstract_unstemmed	Background Neuroblastoma (NB) is an extra-cranial solid tumour of childhood. In spite of the good clinical response to first-line therapy, complete eradication of NB cells is rarely achieved. Thus, new therapeutic strategies are needed to eradicate surviving NB cells and prevent relapse. Sodium ascorbate has been recently reported to induce apoptosis of B16 melanoma cells through down-regulation of the transferrin receptor, CD71. Since NB and melanoma share the same embryologic neuroectodermal origin, we used different human NB cell lines to assess whether the same findings occurred. Results We could observe dose- and time-dependent induction of apoptosis in all NB cell lines. Sodium ascorbate decreased the expression of CD71 and caused cell death within 24 h. An increase in the global and specific caspase activity took place, as well as an early loss of the mitochondrial transmembrane potential. Moreover, intracellular iron was significantly decreased after exposure to sodium ascorbate. Apoptotic markers were reverted when the cells were pretreated with the iron donor ferric ammonium citrate (FAC), further confirming that iron depletion is responsible for the ascorbate-induced cell death in NB cells. Conclusion Sodium ascorbate is highly toxic to neuroblastoma cell lines and the specific mechanism of vitamin C-induced apoptosis is due to a perturbation of intracellular iron levels ensuing TfR-downregulation. © Carosio et al; licensee BioMed Central Ltd. 2007
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title_short	Sodium Ascorbate induces apoptosis in neuroblastoma cell lines by interfering with iron uptake
url	https://dx.doi.org/10.1186/1476-4598-6-55
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up_date	2024-07-03T22:17:16.735Z
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Sodium Ascorbate induces apoptosis in neuroblastoma cell lines by interfering with iron uptake

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Zugang & Verfügbarkeit

Vorhandene Bände

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