Benzo[a]pyrene diol epoxide suppresses retinoic acid receptor-$ β_{2} $ expression by recruiting DNA (cytosine-5-)-methyltransferase 3A

Abstract Tobacco smoke is an important risk factor for various human cancers, including esophageal cancer. How benzo [a]pyrene diol epoxide (BPDE), a carcinogen present in tobacco smoke as well as in environmental pollution, induces esophageal carcinogenesis has yet to be defined. In this study, we...
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Gespeichert in:

Autor*in:	Ye, Fei [verfasserIn] Xu, Xiao-Chun

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2010

Schlagwörter:	Esophageal Cancer Esophageal Cancer Cell Esophageal Epithelial Cell Esophageal Cancer Cell Line Tobacco Carcinogen

Anmerkung:	© Ye and Xu; licensee BioMed Central Ltd. 2010

Übergeordnetes Werk:	Enthalten in: Molecular cancer - London : Biomed Central, 2002, 9(2010), 1 vom: 28. Apr.
Übergeordnetes Werk:	volume:9 ; year:2010 ; number:1 ; day:28 ; month:04

Links:	Volltext

DOI / URN:	10.1186/1476-4598-9-93

Katalog-ID:	SPR028919726

Internformat


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520			\|a Abstract Tobacco smoke is an important risk factor for various human cancers, including esophageal cancer. How benzo [a]pyrene diol epoxide (BPDE), a carcinogen present in tobacco smoke as well as in environmental pollution, induces esophageal carcinogenesis has yet to be defined. In this study, we investigated the molecular mechanism responsible for BPDE-suppressed expression of retinoic acid receptor-beta2 (RAR-$ β_{2} $) in esophageal cancer cells. We treated esophageal cancer cells with BPDE before performing methylation-specific polymerase chain reaction (MSP) to find that BPDE induced methylation of the RAR-$ β_{2} $ gene promoter. We then performed chromatin immunoprecipitation (ChIP) assays to find that BPDE recruited genes of the methylation machinery into the RAR-$ β_{2} $ gene promoter. We found that BPDE recruited DNA (cytosine-5-)-methyltransferase 3 alpha (DNMT3A), but not beta (DNMT3B), in a time-dependent manner to methylate the RAR-$ β_{2} $ gene promoter, which we confirmed by reverse transcription-polymerase chain reaction (RT-PCR) analysis of the reduced RAR-$ β_{2} $ expression in these BPDE-treated esophageal cancer cell lines. However, BPDE did not significantly change DNMT3A expression, but it slightly reduced DNMT3B expression. DNA methylase inhibitor 5-aza-2'-deoxycytidine (5-Aza) and DNMT3A small hairpin RNA (shRNA) vector antagonized the effects of BPDE on RAR-$ β_{2} $ expressions. Transient transfection of the DNMT3A shRNA vector also antagonized BPDE's effects on expression of RAR-$ β_{2} $, c-Jun, phosphorylated extracellular signal-regulated protein kinases 1/2 (ERK1/2), and cyclooxygenase-2 (COX-2), suggesting a possible therapeutic effect. The results of this study form the link between the esophageal cancer risk factor BPDE and the reduced RAR-$ β_{2} $ expression.
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publishDate	2010
allfields	10.1186/1476-4598-9-93 doi (DE-627)SPR028919726 (SPR)1476-4598-9-93-e DE-627 ger DE-627 rakwb eng Ye, Fei verfasserin aut Benzo[a]pyrene diol epoxide suppresses retinoic acid receptor-$ β_{2} $ expression by recruiting DNA (cytosine-5-)-methyltransferase 3A 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Ye and Xu; licensee BioMed Central Ltd. 2010 Abstract Tobacco smoke is an important risk factor for various human cancers, including esophageal cancer. How benzo [a]pyrene diol epoxide (BPDE), a carcinogen present in tobacco smoke as well as in environmental pollution, induces esophageal carcinogenesis has yet to be defined. In this study, we investigated the molecular mechanism responsible for BPDE-suppressed expression of retinoic acid receptor-beta2 (RAR-$ β_{2} $) in esophageal cancer cells. We treated esophageal cancer cells with BPDE before performing methylation-specific polymerase chain reaction (MSP) to find that BPDE induced methylation of the RAR-$ β_{2} $ gene promoter. We then performed chromatin immunoprecipitation (ChIP) assays to find that BPDE recruited genes of the methylation machinery into the RAR-$ β_{2} $ gene promoter. We found that BPDE recruited DNA (cytosine-5-)-methyltransferase 3 alpha (DNMT3A), but not beta (DNMT3B), in a time-dependent manner to methylate the RAR-$ β_{2} $ gene promoter, which we confirmed by reverse transcription-polymerase chain reaction (RT-PCR) analysis of the reduced RAR-$ β_{2} $ expression in these BPDE-treated esophageal cancer cell lines. However, BPDE did not significantly change DNMT3A expression, but it slightly reduced DNMT3B expression. DNA methylase inhibitor 5-aza-2'-deoxycytidine (5-Aza) and DNMT3A small hairpin RNA (shRNA) vector antagonized the effects of BPDE on RAR-$ β_{2} $ expressions. Transient transfection of the DNMT3A shRNA vector also antagonized BPDE's effects on expression of RAR-$ β_{2} $, c-Jun, phosphorylated extracellular signal-regulated protein kinases 1/2 (ERK1/2), and cyclooxygenase-2 (COX-2), suggesting a possible therapeutic effect. The results of this study form the link between the esophageal cancer risk factor BPDE and the reduced RAR-$ β_{2} $ expression. Esophageal Cancer (dpeaa)DE-He213 Esophageal Cancer Cell (dpeaa)DE-He213 Esophageal Epithelial Cell (dpeaa)DE-He213 Esophageal Cancer Cell Line (dpeaa)DE-He213 Tobacco Carcinogen (dpeaa)DE-He213 Xu, Xiao-Chun aut Enthalten in Molecular cancer London : Biomed Central, 2002 9(2010), 1 vom: 28. Apr. (DE-627)355987619 (DE-600)2091373-4 1476-4598 nnns volume:9 year:2010 number:1 day:28 month:04 https://dx.doi.org/10.1186/1476-4598-9-93 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 9 2010 1 28 04
spelling	10.1186/1476-4598-9-93 doi (DE-627)SPR028919726 (SPR)1476-4598-9-93-e DE-627 ger DE-627 rakwb eng Ye, Fei verfasserin aut Benzo[a]pyrene diol epoxide suppresses retinoic acid receptor-$ β_{2} $ expression by recruiting DNA (cytosine-5-)-methyltransferase 3A 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Ye and Xu; licensee BioMed Central Ltd. 2010 Abstract Tobacco smoke is an important risk factor for various human cancers, including esophageal cancer. How benzo [a]pyrene diol epoxide (BPDE), a carcinogen present in tobacco smoke as well as in environmental pollution, induces esophageal carcinogenesis has yet to be defined. In this study, we investigated the molecular mechanism responsible for BPDE-suppressed expression of retinoic acid receptor-beta2 (RAR-$ β_{2} $) in esophageal cancer cells. We treated esophageal cancer cells with BPDE before performing methylation-specific polymerase chain reaction (MSP) to find that BPDE induced methylation of the RAR-$ β_{2} $ gene promoter. We then performed chromatin immunoprecipitation (ChIP) assays to find that BPDE recruited genes of the methylation machinery into the RAR-$ β_{2} $ gene promoter. We found that BPDE recruited DNA (cytosine-5-)-methyltransferase 3 alpha (DNMT3A), but not beta (DNMT3B), in a time-dependent manner to methylate the RAR-$ β_{2} $ gene promoter, which we confirmed by reverse transcription-polymerase chain reaction (RT-PCR) analysis of the reduced RAR-$ β_{2} $ expression in these BPDE-treated esophageal cancer cell lines. However, BPDE did not significantly change DNMT3A expression, but it slightly reduced DNMT3B expression. DNA methylase inhibitor 5-aza-2'-deoxycytidine (5-Aza) and DNMT3A small hairpin RNA (shRNA) vector antagonized the effects of BPDE on RAR-$ β_{2} $ expressions. Transient transfection of the DNMT3A shRNA vector also antagonized BPDE's effects on expression of RAR-$ β_{2} $, c-Jun, phosphorylated extracellular signal-regulated protein kinases 1/2 (ERK1/2), and cyclooxygenase-2 (COX-2), suggesting a possible therapeutic effect. The results of this study form the link between the esophageal cancer risk factor BPDE and the reduced RAR-$ β_{2} $ expression. Esophageal Cancer (dpeaa)DE-He213 Esophageal Cancer Cell (dpeaa)DE-He213 Esophageal Epithelial Cell (dpeaa)DE-He213 Esophageal Cancer Cell Line (dpeaa)DE-He213 Tobacco Carcinogen (dpeaa)DE-He213 Xu, Xiao-Chun aut Enthalten in Molecular cancer London : Biomed Central, 2002 9(2010), 1 vom: 28. Apr. (DE-627)355987619 (DE-600)2091373-4 1476-4598 nnns volume:9 year:2010 number:1 day:28 month:04 https://dx.doi.org/10.1186/1476-4598-9-93 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 9 2010 1 28 04
allfields_unstemmed	10.1186/1476-4598-9-93 doi (DE-627)SPR028919726 (SPR)1476-4598-9-93-e DE-627 ger DE-627 rakwb eng Ye, Fei verfasserin aut Benzo[a]pyrene diol epoxide suppresses retinoic acid receptor-$ β_{2} $ expression by recruiting DNA (cytosine-5-)-methyltransferase 3A 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Ye and Xu; licensee BioMed Central Ltd. 2010 Abstract Tobacco smoke is an important risk factor for various human cancers, including esophageal cancer. How benzo [a]pyrene diol epoxide (BPDE), a carcinogen present in tobacco smoke as well as in environmental pollution, induces esophageal carcinogenesis has yet to be defined. In this study, we investigated the molecular mechanism responsible for BPDE-suppressed expression of retinoic acid receptor-beta2 (RAR-$ β_{2} $) in esophageal cancer cells. We treated esophageal cancer cells with BPDE before performing methylation-specific polymerase chain reaction (MSP) to find that BPDE induced methylation of the RAR-$ β_{2} $ gene promoter. We then performed chromatin immunoprecipitation (ChIP) assays to find that BPDE recruited genes of the methylation machinery into the RAR-$ β_{2} $ gene promoter. We found that BPDE recruited DNA (cytosine-5-)-methyltransferase 3 alpha (DNMT3A), but not beta (DNMT3B), in a time-dependent manner to methylate the RAR-$ β_{2} $ gene promoter, which we confirmed by reverse transcription-polymerase chain reaction (RT-PCR) analysis of the reduced RAR-$ β_{2} $ expression in these BPDE-treated esophageal cancer cell lines. However, BPDE did not significantly change DNMT3A expression, but it slightly reduced DNMT3B expression. DNA methylase inhibitor 5-aza-2'-deoxycytidine (5-Aza) and DNMT3A small hairpin RNA (shRNA) vector antagonized the effects of BPDE on RAR-$ β_{2} $ expressions. Transient transfection of the DNMT3A shRNA vector also antagonized BPDE's effects on expression of RAR-$ β_{2} $, c-Jun, phosphorylated extracellular signal-regulated protein kinases 1/2 (ERK1/2), and cyclooxygenase-2 (COX-2), suggesting a possible therapeutic effect. The results of this study form the link between the esophageal cancer risk factor BPDE and the reduced RAR-$ β_{2} $ expression. Esophageal Cancer (dpeaa)DE-He213 Esophageal Cancer Cell (dpeaa)DE-He213 Esophageal Epithelial Cell (dpeaa)DE-He213 Esophageal Cancer Cell Line (dpeaa)DE-He213 Tobacco Carcinogen (dpeaa)DE-He213 Xu, Xiao-Chun aut Enthalten in Molecular cancer London : Biomed Central, 2002 9(2010), 1 vom: 28. Apr. (DE-627)355987619 (DE-600)2091373-4 1476-4598 nnns volume:9 year:2010 number:1 day:28 month:04 https://dx.doi.org/10.1186/1476-4598-9-93 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 9 2010 1 28 04
allfieldsGer	10.1186/1476-4598-9-93 doi (DE-627)SPR028919726 (SPR)1476-4598-9-93-e DE-627 ger DE-627 rakwb eng Ye, Fei verfasserin aut Benzo[a]pyrene diol epoxide suppresses retinoic acid receptor-$ β_{2} $ expression by recruiting DNA (cytosine-5-)-methyltransferase 3A 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Ye and Xu; licensee BioMed Central Ltd. 2010 Abstract Tobacco smoke is an important risk factor for various human cancers, including esophageal cancer. How benzo [a]pyrene diol epoxide (BPDE), a carcinogen present in tobacco smoke as well as in environmental pollution, induces esophageal carcinogenesis has yet to be defined. In this study, we investigated the molecular mechanism responsible for BPDE-suppressed expression of retinoic acid receptor-beta2 (RAR-$ β_{2} $) in esophageal cancer cells. We treated esophageal cancer cells with BPDE before performing methylation-specific polymerase chain reaction (MSP) to find that BPDE induced methylation of the RAR-$ β_{2} $ gene promoter. We then performed chromatin immunoprecipitation (ChIP) assays to find that BPDE recruited genes of the methylation machinery into the RAR-$ β_{2} $ gene promoter. We found that BPDE recruited DNA (cytosine-5-)-methyltransferase 3 alpha (DNMT3A), but not beta (DNMT3B), in a time-dependent manner to methylate the RAR-$ β_{2} $ gene promoter, which we confirmed by reverse transcription-polymerase chain reaction (RT-PCR) analysis of the reduced RAR-$ β_{2} $ expression in these BPDE-treated esophageal cancer cell lines. However, BPDE did not significantly change DNMT3A expression, but it slightly reduced DNMT3B expression. DNA methylase inhibitor 5-aza-2'-deoxycytidine (5-Aza) and DNMT3A small hairpin RNA (shRNA) vector antagonized the effects of BPDE on RAR-$ β_{2} $ expressions. Transient transfection of the DNMT3A shRNA vector also antagonized BPDE's effects on expression of RAR-$ β_{2} $, c-Jun, phosphorylated extracellular signal-regulated protein kinases 1/2 (ERK1/2), and cyclooxygenase-2 (COX-2), suggesting a possible therapeutic effect. The results of this study form the link between the esophageal cancer risk factor BPDE and the reduced RAR-$ β_{2} $ expression. Esophageal Cancer (dpeaa)DE-He213 Esophageal Cancer Cell (dpeaa)DE-He213 Esophageal Epithelial Cell (dpeaa)DE-He213 Esophageal Cancer Cell Line (dpeaa)DE-He213 Tobacco Carcinogen (dpeaa)DE-He213 Xu, Xiao-Chun aut Enthalten in Molecular cancer London : Biomed Central, 2002 9(2010), 1 vom: 28. Apr. (DE-627)355987619 (DE-600)2091373-4 1476-4598 nnns volume:9 year:2010 number:1 day:28 month:04 https://dx.doi.org/10.1186/1476-4598-9-93 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 9 2010 1 28 04
allfieldsSound	10.1186/1476-4598-9-93 doi (DE-627)SPR028919726 (SPR)1476-4598-9-93-e DE-627 ger DE-627 rakwb eng Ye, Fei verfasserin aut Benzo[a]pyrene diol epoxide suppresses retinoic acid receptor-$ β_{2} $ expression by recruiting DNA (cytosine-5-)-methyltransferase 3A 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Ye and Xu; licensee BioMed Central Ltd. 2010 Abstract Tobacco smoke is an important risk factor for various human cancers, including esophageal cancer. How benzo [a]pyrene diol epoxide (BPDE), a carcinogen present in tobacco smoke as well as in environmental pollution, induces esophageal carcinogenesis has yet to be defined. In this study, we investigated the molecular mechanism responsible for BPDE-suppressed expression of retinoic acid receptor-beta2 (RAR-$ β_{2} $) in esophageal cancer cells. We treated esophageal cancer cells with BPDE before performing methylation-specific polymerase chain reaction (MSP) to find that BPDE induced methylation of the RAR-$ β_{2} $ gene promoter. We then performed chromatin immunoprecipitation (ChIP) assays to find that BPDE recruited genes of the methylation machinery into the RAR-$ β_{2} $ gene promoter. We found that BPDE recruited DNA (cytosine-5-)-methyltransferase 3 alpha (DNMT3A), but not beta (DNMT3B), in a time-dependent manner to methylate the RAR-$ β_{2} $ gene promoter, which we confirmed by reverse transcription-polymerase chain reaction (RT-PCR) analysis of the reduced RAR-$ β_{2} $ expression in these BPDE-treated esophageal cancer cell lines. However, BPDE did not significantly change DNMT3A expression, but it slightly reduced DNMT3B expression. DNA methylase inhibitor 5-aza-2'-deoxycytidine (5-Aza) and DNMT3A small hairpin RNA (shRNA) vector antagonized the effects of BPDE on RAR-$ β_{2} $ expressions. Transient transfection of the DNMT3A shRNA vector also antagonized BPDE's effects on expression of RAR-$ β_{2} $, c-Jun, phosphorylated extracellular signal-regulated protein kinases 1/2 (ERK1/2), and cyclooxygenase-2 (COX-2), suggesting a possible therapeutic effect. The results of this study form the link between the esophageal cancer risk factor BPDE and the reduced RAR-$ β_{2} $ expression. Esophageal Cancer (dpeaa)DE-He213 Esophageal Cancer Cell (dpeaa)DE-He213 Esophageal Epithelial Cell (dpeaa)DE-He213 Esophageal Cancer Cell Line (dpeaa)DE-He213 Tobacco Carcinogen (dpeaa)DE-He213 Xu, Xiao-Chun aut Enthalten in Molecular cancer London : Biomed Central, 2002 9(2010), 1 vom: 28. Apr. (DE-627)355987619 (DE-600)2091373-4 1476-4598 nnns volume:9 year:2010 number:1 day:28 month:04 https://dx.doi.org/10.1186/1476-4598-9-93 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 9 2010 1 28 04
language	English
source	Enthalten in Molecular cancer 9(2010), 1 vom: 28. Apr. volume:9 year:2010 number:1 day:28 month:04
sourceStr	Enthalten in Molecular cancer 9(2010), 1 vom: 28. Apr. volume:9 year:2010 number:1 day:28 month:04
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Esophageal Cancer Esophageal Cancer Cell Esophageal Epithelial Cell Esophageal Cancer Cell Line Tobacco Carcinogen
isfreeaccess_bool	true
container_title	Molecular cancer
authorswithroles_txt_mv	Ye, Fei @@aut@@ Xu, Xiao-Chun @@aut@@
publishDateDaySort_date	2010-04-28T00:00:00Z
hierarchy_top_id	355987619
id	SPR028919726
language_de	englisch
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author	Ye, Fei
spellingShingle	Ye, Fei misc Esophageal Cancer misc Esophageal Cancer Cell misc Esophageal Epithelial Cell misc Esophageal Cancer Cell Line misc Tobacco Carcinogen Benzo[a]pyrene diol epoxide suppresses retinoic acid receptor-$ β_{2} $ expression by recruiting DNA (cytosine-5-)-methyltransferase 3A
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topic_title	Benzo[a]pyrene diol epoxide suppresses retinoic acid receptor-$ β_{2} $ expression by recruiting DNA (cytosine-5-)-methyltransferase 3A Esophageal Cancer (dpeaa)DE-He213 Esophageal Cancer Cell (dpeaa)DE-He213 Esophageal Epithelial Cell (dpeaa)DE-He213 Esophageal Cancer Cell Line (dpeaa)DE-He213 Tobacco Carcinogen (dpeaa)DE-He213
topic	misc Esophageal Cancer misc Esophageal Cancer Cell misc Esophageal Epithelial Cell misc Esophageal Cancer Cell Line misc Tobacco Carcinogen
topic_unstemmed	misc Esophageal Cancer misc Esophageal Cancer Cell misc Esophageal Epithelial Cell misc Esophageal Cancer Cell Line misc Tobacco Carcinogen
topic_browse	misc Esophageal Cancer misc Esophageal Cancer Cell misc Esophageal Epithelial Cell misc Esophageal Cancer Cell Line misc Tobacco Carcinogen
format_facet	Elektronische Aufsätze Aufsätze Elektronische Ressource
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title	Benzo[a]pyrene diol epoxide suppresses retinoic acid receptor-$ β_{2} $ expression by recruiting DNA (cytosine-5-)-methyltransferase 3A
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title_full	Benzo[a]pyrene diol epoxide suppresses retinoic acid receptor-$ β_{2} $ expression by recruiting DNA (cytosine-5-)-methyltransferase 3A
author_sort	Ye, Fei
journal	Molecular cancer
journalStr	Molecular cancer
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author_browse	Ye, Fei Xu, Xiao-Chun
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format_se	Elektronische Aufsätze
author-letter	Ye, Fei
doi_str_mv	10.1186/1476-4598-9-93
title_sort	benzo[a]pyrene diol epoxide suppresses retinoic acid receptor-$ β_{2} $ expression by recruiting dna (cytosine-5-)-methyltransferase 3a
title_auth	Benzo[a]pyrene diol epoxide suppresses retinoic acid receptor-$ β_{2} $ expression by recruiting DNA (cytosine-5-)-methyltransferase 3A
abstract	Abstract Tobacco smoke is an important risk factor for various human cancers, including esophageal cancer. How benzo [a]pyrene diol epoxide (BPDE), a carcinogen present in tobacco smoke as well as in environmental pollution, induces esophageal carcinogenesis has yet to be defined. In this study, we investigated the molecular mechanism responsible for BPDE-suppressed expression of retinoic acid receptor-beta2 (RAR-$ β_{2} $) in esophageal cancer cells. We treated esophageal cancer cells with BPDE before performing methylation-specific polymerase chain reaction (MSP) to find that BPDE induced methylation of the RAR-$ β_{2} $ gene promoter. We then performed chromatin immunoprecipitation (ChIP) assays to find that BPDE recruited genes of the methylation machinery into the RAR-$ β_{2} $ gene promoter. We found that BPDE recruited DNA (cytosine-5-)-methyltransferase 3 alpha (DNMT3A), but not beta (DNMT3B), in a time-dependent manner to methylate the RAR-$ β_{2} $ gene promoter, which we confirmed by reverse transcription-polymerase chain reaction (RT-PCR) analysis of the reduced RAR-$ β_{2} $ expression in these BPDE-treated esophageal cancer cell lines. However, BPDE did not significantly change DNMT3A expression, but it slightly reduced DNMT3B expression. DNA methylase inhibitor 5-aza-2'-deoxycytidine (5-Aza) and DNMT3A small hairpin RNA (shRNA) vector antagonized the effects of BPDE on RAR-$ β_{2} $ expressions. Transient transfection of the DNMT3A shRNA vector also antagonized BPDE's effects on expression of RAR-$ β_{2} $, c-Jun, phosphorylated extracellular signal-regulated protein kinases 1/2 (ERK1/2), and cyclooxygenase-2 (COX-2), suggesting a possible therapeutic effect. The results of this study form the link between the esophageal cancer risk factor BPDE and the reduced RAR-$ β_{2} $ expression. © Ye and Xu; licensee BioMed Central Ltd. 2010
abstractGer	Abstract Tobacco smoke is an important risk factor for various human cancers, including esophageal cancer. How benzo [a]pyrene diol epoxide (BPDE), a carcinogen present in tobacco smoke as well as in environmental pollution, induces esophageal carcinogenesis has yet to be defined. In this study, we investigated the molecular mechanism responsible for BPDE-suppressed expression of retinoic acid receptor-beta2 (RAR-$ β_{2} $) in esophageal cancer cells. We treated esophageal cancer cells with BPDE before performing methylation-specific polymerase chain reaction (MSP) to find that BPDE induced methylation of the RAR-$ β_{2} $ gene promoter. We then performed chromatin immunoprecipitation (ChIP) assays to find that BPDE recruited genes of the methylation machinery into the RAR-$ β_{2} $ gene promoter. We found that BPDE recruited DNA (cytosine-5-)-methyltransferase 3 alpha (DNMT3A), but not beta (DNMT3B), in a time-dependent manner to methylate the RAR-$ β_{2} $ gene promoter, which we confirmed by reverse transcription-polymerase chain reaction (RT-PCR) analysis of the reduced RAR-$ β_{2} $ expression in these BPDE-treated esophageal cancer cell lines. However, BPDE did not significantly change DNMT3A expression, but it slightly reduced DNMT3B expression. DNA methylase inhibitor 5-aza-2'-deoxycytidine (5-Aza) and DNMT3A small hairpin RNA (shRNA) vector antagonized the effects of BPDE on RAR-$ β_{2} $ expressions. Transient transfection of the DNMT3A shRNA vector also antagonized BPDE's effects on expression of RAR-$ β_{2} $, c-Jun, phosphorylated extracellular signal-regulated protein kinases 1/2 (ERK1/2), and cyclooxygenase-2 (COX-2), suggesting a possible therapeutic effect. The results of this study form the link between the esophageal cancer risk factor BPDE and the reduced RAR-$ β_{2} $ expression. © Ye and Xu; licensee BioMed Central Ltd. 2010
abstract_unstemmed	Abstract Tobacco smoke is an important risk factor for various human cancers, including esophageal cancer. How benzo [a]pyrene diol epoxide (BPDE), a carcinogen present in tobacco smoke as well as in environmental pollution, induces esophageal carcinogenesis has yet to be defined. In this study, we investigated the molecular mechanism responsible for BPDE-suppressed expression of retinoic acid receptor-beta2 (RAR-$ β_{2} $) in esophageal cancer cells. We treated esophageal cancer cells with BPDE before performing methylation-specific polymerase chain reaction (MSP) to find that BPDE induced methylation of the RAR-$ β_{2} $ gene promoter. We then performed chromatin immunoprecipitation (ChIP) assays to find that BPDE recruited genes of the methylation machinery into the RAR-$ β_{2} $ gene promoter. We found that BPDE recruited DNA (cytosine-5-)-methyltransferase 3 alpha (DNMT3A), but not beta (DNMT3B), in a time-dependent manner to methylate the RAR-$ β_{2} $ gene promoter, which we confirmed by reverse transcription-polymerase chain reaction (RT-PCR) analysis of the reduced RAR-$ β_{2} $ expression in these BPDE-treated esophageal cancer cell lines. However, BPDE did not significantly change DNMT3A expression, but it slightly reduced DNMT3B expression. DNA methylase inhibitor 5-aza-2'-deoxycytidine (5-Aza) and DNMT3A small hairpin RNA (shRNA) vector antagonized the effects of BPDE on RAR-$ β_{2} $ expressions. Transient transfection of the DNMT3A shRNA vector also antagonized BPDE's effects on expression of RAR-$ β_{2} $, c-Jun, phosphorylated extracellular signal-regulated protein kinases 1/2 (ERK1/2), and cyclooxygenase-2 (COX-2), suggesting a possible therapeutic effect. The results of this study form the link between the esophageal cancer risk factor BPDE and the reduced RAR-$ β_{2} $ expression. © Ye and Xu; licensee BioMed Central Ltd. 2010
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title_short	Benzo[a]pyrene diol epoxide suppresses retinoic acid receptor-$ β_{2} $ expression by recruiting DNA (cytosine-5-)-methyltransferase 3A
url	https://dx.doi.org/10.1186/1476-4598-9-93
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Benzo[a]pyrene diol epoxide suppresses retinoic acid receptor-$ β_{2} $ expression by recruiting DNA (cytosine-5-)-methyltransferase 3A

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