Targeting metabolism with arsenic trioxide and dichloroacetate in breast cancer cells

<p<Abstract</p< <p<Background</p< <p<Cancer cells have a different metabolic profile compared to normal cells. The Warburg effect (increased aerobic glycolysis) and glutaminolysis (increased mitochondrial activity from glutamine catabolism) are well known hallmarks of c...
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Autor*in:	Sun Ramon C [verfasserIn] Board Philip G [verfasserIn] Blackburn Anneke C [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2011

Schlagwörter:	Dichloroacetate breast cancer electron transport chain mitochondria arsenic trioxide

Übergeordnetes Werk:	In: Molecular Cancer - BMC, 2003, 10(2011), 1, p 142
Übergeordnetes Werk:	volume:10 ; year:2011 ; number:1, p 142

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1186/1476-4598-10-142

Katalog-ID:	DOAJ026072408

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allfields	10.1186/1476-4598-10-142 doi (DE-627)DOAJ026072408 (DE-599)DOAJ5ed3885bb0a14a1f8484669ab009a3d5 DE-627 ger DE-627 rakwb eng RC254-282 Sun Ramon C verfasserin aut Targeting metabolism with arsenic trioxide and dichloroacetate in breast cancer cells 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<Cancer cells have a different metabolic profile compared to normal cells. The Warburg effect (increased aerobic glycolysis) and glutaminolysis (increased mitochondrial activity from glutamine catabolism) are well known hallmarks of cancer and are accompanied by increased lactate production, hyperpolarized mitochondrial membrane and increased production of reactive oxygen species.</p< <p<Methods</p< <p<In this study we target the Warburg effect with dichloroacetate (DCA) and the increased mitochondrial activity of glutaminolysis with arsenic trioxide (ATO) in breast cancer cells, measuring cell proliferation, cell death and mitochondrial characteristics.</p< <p<Results</p< <p<The combination of DCA and ATO was more effective at inhibiting cell proliferation and inducing cell death than either drug alone. We examined the effect of these treatments on mitochondrial membrane potential, reactive oxygen species production and ATP levels and have identified new molecular mechanisms within the mitochondria for both ATO and DCA: ATO reduces mitochondrial function through the inhibition of cytochrome C oxidase (complex IV of the electron transport chain) while DCA up-regulates ATP synthase β subunit expression. The potentiation of ATO cytotoxicity by DCA is correlated with strong suppression of the expression of c-Myc and HIF-1α, and decreased expression of the survival protein Bcl-2.</p< <p<Conclusion</p< <p<This study is the first to demonstrate that targeting two key metabolic hallmarks of cancer is an effective anti-cancer strategy with therapeutic potential.</p< Dichloroacetate breast cancer electron transport chain mitochondria arsenic trioxide Neoplasms. Tumors. Oncology. Including cancer and carcinogens Board Philip G verfasserin aut Blackburn Anneke C verfasserin aut In Molecular Cancer BMC, 2003 10(2011), 1, p 142 (DE-627)355987619 (DE-600)2091373-4 14764598 nnns volume:10 year:2011 number:1, p 142 https://doi.org/10.1186/1476-4598-10-142 kostenfrei https://doaj.org/article/5ed3885bb0a14a1f8484669ab009a3d5 kostenfrei http://www.molecular-cancer.com/content/10/1/142 kostenfrei https://doaj.org/toc/1476-4598 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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 10 2011 1, p 142
spelling	10.1186/1476-4598-10-142 doi (DE-627)DOAJ026072408 (DE-599)DOAJ5ed3885bb0a14a1f8484669ab009a3d5 DE-627 ger DE-627 rakwb eng RC254-282 Sun Ramon C verfasserin aut Targeting metabolism with arsenic trioxide and dichloroacetate in breast cancer cells 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<Cancer cells have a different metabolic profile compared to normal cells. The Warburg effect (increased aerobic glycolysis) and glutaminolysis (increased mitochondrial activity from glutamine catabolism) are well known hallmarks of cancer and are accompanied by increased lactate production, hyperpolarized mitochondrial membrane and increased production of reactive oxygen species.</p< <p<Methods</p< <p<In this study we target the Warburg effect with dichloroacetate (DCA) and the increased mitochondrial activity of glutaminolysis with arsenic trioxide (ATO) in breast cancer cells, measuring cell proliferation, cell death and mitochondrial characteristics.</p< <p<Results</p< <p<The combination of DCA and ATO was more effective at inhibiting cell proliferation and inducing cell death than either drug alone. We examined the effect of these treatments on mitochondrial membrane potential, reactive oxygen species production and ATP levels and have identified new molecular mechanisms within the mitochondria for both ATO and DCA: ATO reduces mitochondrial function through the inhibition of cytochrome C oxidase (complex IV of the electron transport chain) while DCA up-regulates ATP synthase β subunit expression. The potentiation of ATO cytotoxicity by DCA is correlated with strong suppression of the expression of c-Myc and HIF-1α, and decreased expression of the survival protein Bcl-2.</p< <p<Conclusion</p< <p<This study is the first to demonstrate that targeting two key metabolic hallmarks of cancer is an effective anti-cancer strategy with therapeutic potential.</p< Dichloroacetate breast cancer electron transport chain mitochondria arsenic trioxide Neoplasms. Tumors. Oncology. Including cancer and carcinogens Board Philip G verfasserin aut Blackburn Anneke C verfasserin aut In Molecular Cancer BMC, 2003 10(2011), 1, p 142 (DE-627)355987619 (DE-600)2091373-4 14764598 nnns volume:10 year:2011 number:1, p 142 https://doi.org/10.1186/1476-4598-10-142 kostenfrei https://doaj.org/article/5ed3885bb0a14a1f8484669ab009a3d5 kostenfrei http://www.molecular-cancer.com/content/10/1/142 kostenfrei https://doaj.org/toc/1476-4598 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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 10 2011 1, p 142
allfields_unstemmed	10.1186/1476-4598-10-142 doi (DE-627)DOAJ026072408 (DE-599)DOAJ5ed3885bb0a14a1f8484669ab009a3d5 DE-627 ger DE-627 rakwb eng RC254-282 Sun Ramon C verfasserin aut Targeting metabolism with arsenic trioxide and dichloroacetate in breast cancer cells 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<Cancer cells have a different metabolic profile compared to normal cells. The Warburg effect (increased aerobic glycolysis) and glutaminolysis (increased mitochondrial activity from glutamine catabolism) are well known hallmarks of cancer and are accompanied by increased lactate production, hyperpolarized mitochondrial membrane and increased production of reactive oxygen species.</p< <p<Methods</p< <p<In this study we target the Warburg effect with dichloroacetate (DCA) and the increased mitochondrial activity of glutaminolysis with arsenic trioxide (ATO) in breast cancer cells, measuring cell proliferation, cell death and mitochondrial characteristics.</p< <p<Results</p< <p<The combination of DCA and ATO was more effective at inhibiting cell proliferation and inducing cell death than either drug alone. We examined the effect of these treatments on mitochondrial membrane potential, reactive oxygen species production and ATP levels and have identified new molecular mechanisms within the mitochondria for both ATO and DCA: ATO reduces mitochondrial function through the inhibition of cytochrome C oxidase (complex IV of the electron transport chain) while DCA up-regulates ATP synthase β subunit expression. The potentiation of ATO cytotoxicity by DCA is correlated with strong suppression of the expression of c-Myc and HIF-1α, and decreased expression of the survival protein Bcl-2.</p< <p<Conclusion</p< <p<This study is the first to demonstrate that targeting two key metabolic hallmarks of cancer is an effective anti-cancer strategy with therapeutic potential.</p< Dichloroacetate breast cancer electron transport chain mitochondria arsenic trioxide Neoplasms. Tumors. Oncology. Including cancer and carcinogens Board Philip G verfasserin aut Blackburn Anneke C verfasserin aut In Molecular Cancer BMC, 2003 10(2011), 1, p 142 (DE-627)355987619 (DE-600)2091373-4 14764598 nnns volume:10 year:2011 number:1, p 142 https://doi.org/10.1186/1476-4598-10-142 kostenfrei https://doaj.org/article/5ed3885bb0a14a1f8484669ab009a3d5 kostenfrei http://www.molecular-cancer.com/content/10/1/142 kostenfrei https://doaj.org/toc/1476-4598 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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 10 2011 1, p 142
allfieldsGer	10.1186/1476-4598-10-142 doi (DE-627)DOAJ026072408 (DE-599)DOAJ5ed3885bb0a14a1f8484669ab009a3d5 DE-627 ger DE-627 rakwb eng RC254-282 Sun Ramon C verfasserin aut Targeting metabolism with arsenic trioxide and dichloroacetate in breast cancer cells 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<Cancer cells have a different metabolic profile compared to normal cells. The Warburg effect (increased aerobic glycolysis) and glutaminolysis (increased mitochondrial activity from glutamine catabolism) are well known hallmarks of cancer and are accompanied by increased lactate production, hyperpolarized mitochondrial membrane and increased production of reactive oxygen species.</p< <p<Methods</p< <p<In this study we target the Warburg effect with dichloroacetate (DCA) and the increased mitochondrial activity of glutaminolysis with arsenic trioxide (ATO) in breast cancer cells, measuring cell proliferation, cell death and mitochondrial characteristics.</p< <p<Results</p< <p<The combination of DCA and ATO was more effective at inhibiting cell proliferation and inducing cell death than either drug alone. We examined the effect of these treatments on mitochondrial membrane potential, reactive oxygen species production and ATP levels and have identified new molecular mechanisms within the mitochondria for both ATO and DCA: ATO reduces mitochondrial function through the inhibition of cytochrome C oxidase (complex IV of the electron transport chain) while DCA up-regulates ATP synthase β subunit expression. The potentiation of ATO cytotoxicity by DCA is correlated with strong suppression of the expression of c-Myc and HIF-1α, and decreased expression of the survival protein Bcl-2.</p< <p<Conclusion</p< <p<This study is the first to demonstrate that targeting two key metabolic hallmarks of cancer is an effective anti-cancer strategy with therapeutic potential.</p< Dichloroacetate breast cancer electron transport chain mitochondria arsenic trioxide Neoplasms. Tumors. Oncology. Including cancer and carcinogens Board Philip G verfasserin aut Blackburn Anneke C verfasserin aut In Molecular Cancer BMC, 2003 10(2011), 1, p 142 (DE-627)355987619 (DE-600)2091373-4 14764598 nnns volume:10 year:2011 number:1, p 142 https://doi.org/10.1186/1476-4598-10-142 kostenfrei https://doaj.org/article/5ed3885bb0a14a1f8484669ab009a3d5 kostenfrei http://www.molecular-cancer.com/content/10/1/142 kostenfrei https://doaj.org/toc/1476-4598 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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 10 2011 1, p 142
allfieldsSound	10.1186/1476-4598-10-142 doi (DE-627)DOAJ026072408 (DE-599)DOAJ5ed3885bb0a14a1f8484669ab009a3d5 DE-627 ger DE-627 rakwb eng RC254-282 Sun Ramon C verfasserin aut Targeting metabolism with arsenic trioxide and dichloroacetate in breast cancer cells 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<Cancer cells have a different metabolic profile compared to normal cells. The Warburg effect (increased aerobic glycolysis) and glutaminolysis (increased mitochondrial activity from glutamine catabolism) are well known hallmarks of cancer and are accompanied by increased lactate production, hyperpolarized mitochondrial membrane and increased production of reactive oxygen species.</p< <p<Methods</p< <p<In this study we target the Warburg effect with dichloroacetate (DCA) and the increased mitochondrial activity of glutaminolysis with arsenic trioxide (ATO) in breast cancer cells, measuring cell proliferation, cell death and mitochondrial characteristics.</p< <p<Results</p< <p<The combination of DCA and ATO was more effective at inhibiting cell proliferation and inducing cell death than either drug alone. We examined the effect of these treatments on mitochondrial membrane potential, reactive oxygen species production and ATP levels and have identified new molecular mechanisms within the mitochondria for both ATO and DCA: ATO reduces mitochondrial function through the inhibition of cytochrome C oxidase (complex IV of the electron transport chain) while DCA up-regulates ATP synthase β subunit expression. The potentiation of ATO cytotoxicity by DCA is correlated with strong suppression of the expression of c-Myc and HIF-1α, and decreased expression of the survival protein Bcl-2.</p< <p<Conclusion</p< <p<This study is the first to demonstrate that targeting two key metabolic hallmarks of cancer is an effective anti-cancer strategy with therapeutic potential.</p< Dichloroacetate breast cancer electron transport chain mitochondria arsenic trioxide Neoplasms. Tumors. Oncology. Including cancer and carcinogens Board Philip G verfasserin aut Blackburn Anneke C verfasserin aut In Molecular Cancer BMC, 2003 10(2011), 1, p 142 (DE-627)355987619 (DE-600)2091373-4 14764598 nnns volume:10 year:2011 number:1, p 142 https://doi.org/10.1186/1476-4598-10-142 kostenfrei https://doaj.org/article/5ed3885bb0a14a1f8484669ab009a3d5 kostenfrei http://www.molecular-cancer.com/content/10/1/142 kostenfrei https://doaj.org/toc/1476-4598 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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 10 2011 1, p 142
language	English
source	In Molecular Cancer 10(2011), 1, p 142 volume:10 year:2011 number:1, p 142
sourceStr	In Molecular Cancer 10(2011), 1, p 142 volume:10 year:2011 number:1, p 142
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Dichloroacetate breast cancer electron transport chain mitochondria arsenic trioxide Neoplasms. Tumors. Oncology. Including cancer and carcinogens
isfreeaccess_bool	true
container_title	Molecular Cancer
authorswithroles_txt_mv	Sun Ramon C @@aut@@ Board Philip G @@aut@@ Blackburn Anneke C @@aut@@
publishDateDaySort_date	2011-01-01T00:00:00Z
hierarchy_top_id	355987619
id	DOAJ026072408
language_de	englisch
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callnumber-first	R - Medicine
author	Sun Ramon C
spellingShingle	Sun Ramon C misc RC254-282 misc Dichloroacetate misc breast cancer misc electron transport chain misc mitochondria misc arsenic trioxide misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens Targeting metabolism with arsenic trioxide and dichloroacetate in breast cancer cells
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topic_title	RC254-282 Targeting metabolism with arsenic trioxide and dichloroacetate in breast cancer cells Dichloroacetate breast cancer electron transport chain mitochondria arsenic trioxide
topic	misc RC254-282 misc Dichloroacetate misc breast cancer misc electron transport chain misc mitochondria misc arsenic trioxide misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens
topic_unstemmed	misc RC254-282 misc Dichloroacetate misc breast cancer misc electron transport chain misc mitochondria misc arsenic trioxide misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens
topic_browse	misc RC254-282 misc Dichloroacetate misc breast cancer misc electron transport chain misc mitochondria misc arsenic trioxide misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens
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title	Targeting metabolism with arsenic trioxide and dichloroacetate in breast cancer cells
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title_full	Targeting metabolism with arsenic trioxide and dichloroacetate in breast cancer cells
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author-letter	Sun Ramon C
doi_str_mv	10.1186/1476-4598-10-142
author2-role	verfasserin
title_sort	targeting metabolism with arsenic trioxide and dichloroacetate in breast cancer cells
callnumber	RC254-282
title_auth	Targeting metabolism with arsenic trioxide and dichloroacetate in breast cancer cells
abstract	<p<Abstract</p< <p<Background</p< <p<Cancer cells have a different metabolic profile compared to normal cells. The Warburg effect (increased aerobic glycolysis) and glutaminolysis (increased mitochondrial activity from glutamine catabolism) are well known hallmarks of cancer and are accompanied by increased lactate production, hyperpolarized mitochondrial membrane and increased production of reactive oxygen species.</p< <p<Methods</p< <p<In this study we target the Warburg effect with dichloroacetate (DCA) and the increased mitochondrial activity of glutaminolysis with arsenic trioxide (ATO) in breast cancer cells, measuring cell proliferation, cell death and mitochondrial characteristics.</p< <p<Results</p< <p<The combination of DCA and ATO was more effective at inhibiting cell proliferation and inducing cell death than either drug alone. We examined the effect of these treatments on mitochondrial membrane potential, reactive oxygen species production and ATP levels and have identified new molecular mechanisms within the mitochondria for both ATO and DCA: ATO reduces mitochondrial function through the inhibition of cytochrome C oxidase (complex IV of the electron transport chain) while DCA up-regulates ATP synthase β subunit expression. The potentiation of ATO cytotoxicity by DCA is correlated with strong suppression of the expression of c-Myc and HIF-1α, and decreased expression of the survival protein Bcl-2.</p< <p<Conclusion</p< <p<This study is the first to demonstrate that targeting two key metabolic hallmarks of cancer is an effective anti-cancer strategy with therapeutic potential.</p<
abstractGer	<p<Abstract</p< <p<Background</p< <p<Cancer cells have a different metabolic profile compared to normal cells. The Warburg effect (increased aerobic glycolysis) and glutaminolysis (increased mitochondrial activity from glutamine catabolism) are well known hallmarks of cancer and are accompanied by increased lactate production, hyperpolarized mitochondrial membrane and increased production of reactive oxygen species.</p< <p<Methods</p< <p<In this study we target the Warburg effect with dichloroacetate (DCA) and the increased mitochondrial activity of glutaminolysis with arsenic trioxide (ATO) in breast cancer cells, measuring cell proliferation, cell death and mitochondrial characteristics.</p< <p<Results</p< <p<The combination of DCA and ATO was more effective at inhibiting cell proliferation and inducing cell death than either drug alone. We examined the effect of these treatments on mitochondrial membrane potential, reactive oxygen species production and ATP levels and have identified new molecular mechanisms within the mitochondria for both ATO and DCA: ATO reduces mitochondrial function through the inhibition of cytochrome C oxidase (complex IV of the electron transport chain) while DCA up-regulates ATP synthase β subunit expression. The potentiation of ATO cytotoxicity by DCA is correlated with strong suppression of the expression of c-Myc and HIF-1α, and decreased expression of the survival protein Bcl-2.</p< <p<Conclusion</p< <p<This study is the first to demonstrate that targeting two key metabolic hallmarks of cancer is an effective anti-cancer strategy with therapeutic potential.</p<
abstract_unstemmed	<p<Abstract</p< <p<Background</p< <p<Cancer cells have a different metabolic profile compared to normal cells. The Warburg effect (increased aerobic glycolysis) and glutaminolysis (increased mitochondrial activity from glutamine catabolism) are well known hallmarks of cancer and are accompanied by increased lactate production, hyperpolarized mitochondrial membrane and increased production of reactive oxygen species.</p< <p<Methods</p< <p<In this study we target the Warburg effect with dichloroacetate (DCA) and the increased mitochondrial activity of glutaminolysis with arsenic trioxide (ATO) in breast cancer cells, measuring cell proliferation, cell death and mitochondrial characteristics.</p< <p<Results</p< <p<The combination of DCA and ATO was more effective at inhibiting cell proliferation and inducing cell death than either drug alone. We examined the effect of these treatments on mitochondrial membrane potential, reactive oxygen species production and ATP levels and have identified new molecular mechanisms within the mitochondria for both ATO and DCA: ATO reduces mitochondrial function through the inhibition of cytochrome C oxidase (complex IV of the electron transport chain) while DCA up-regulates ATP synthase β subunit expression. The potentiation of ATO cytotoxicity by DCA is correlated with strong suppression of the expression of c-Myc and HIF-1α, and decreased expression of the survival protein Bcl-2.</p< <p<Conclusion</p< <p<This study is the first to demonstrate that targeting two key metabolic hallmarks of cancer is an effective anti-cancer strategy with therapeutic potential.</p<
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Targeting metabolism with arsenic trioxide and dichloroacetate in breast cancer cells

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