The long non-coding RNA ANRASSF1 in the regulation of alternative protein-coding transcripts RASSF1A and RASSF1C in human breast cancer cells: implications to epigenetic therapy

Alternative protein-coding transcripts of the RASSF1 gene have been associated with dual functions in human cancer: while RASSF1C isoform has oncogenic properties, RASSF1A is a tumour suppressor frequently silenced by hypermethylation. Recently, the antisense long non-coding RNA RASSF1 (ANRASSF1) wa...
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Autor*in:	Naiade Calanca [verfasserIn] Ana Paula Paschoal [verfasserIn] Érika Prando Munhoz [verfasserIn] Layla Testa Galindo [verfasserIn] Barbara Mitsuyasu Barbosa [verfasserIn] José Roberto Fígaro Caldeira [verfasserIn] Rogério Antonio Oliveira [verfasserIn] Luciane Regina Cavalli [verfasserIn] Silvia Regina Rogatto [verfasserIn] Cláudia Aparecida Rainho [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2019

Schlagwörter:	dna methylation rassf1a rassf1c rassf1-as1 lncrna locus-specific epigenetic repression

Übergeordnetes Werk:	In: Epigenetics - Taylor & Francis Group, 2023, 14(2019), 8, Seite 741-750
Übergeordnetes Werk:	volume:14 ; year:2019 ; number:8 ; pages:741-750

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc Journal toc

DOI / URN:	10.1080/15592294.2019.1615355

Katalog-ID:	DOAJ098188739

Internformat


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245	1	4	\|a The long non-coding RNA ANRASSF1 in the regulation of alternative protein-coding transcripts RASSF1A and RASSF1C in human breast cancer cells: implications to epigenetic therapy
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520			\|a Alternative protein-coding transcripts of the RASSF1 gene have been associated with dual functions in human cancer: while RASSF1C isoform has oncogenic properties, RASSF1A is a tumour suppressor frequently silenced by hypermethylation. Recently, the antisense long non-coding RNA RASSF1 (ANRASSF1) was implicated in a locus-specific mechanism for the RASSF1A epigenetic repression mediated by PRC2 (Polycomb Repressive Complex 2). Here, we evaluated the methylation patterns of the promoter regions of RASSF1A and RASSF1C and the expression levels of these RASSF1 transcripts in breast cancer and breast cancer cell lines. As expected, RASSF1C remained unmethylated and RASSF1A was hypermethylated at high frequencies in 75 primary breast cancers, and also in a panel of three mammary epithelial cells (MEC) and 10 breast cancer cell lines (BCC). Although RASSF1C was expressed in all cell lines, only two of them expressed the transcript RASSF1A. ANRASSF1 expression levels were increased in six BCCs. In vitro induced demethylation with 5-Aza-2ʹ-deoxicytydine (5-Aza-dC) resulted in up-regulation of RASSF1A and an inverse correlation with ANRASSF1 relative abundance in BCCs. However, increased levels of both transcripts were observed in two MECs (184A1 and MCF10A) after treatment with 5-Aza-dC. Overall, these findings indicate that ANRASSF1 is differentially expressed in MECs and BCCs. The lncRNA ANRASSF1 provides new perspectives as a therapeutic target for locus-specific regulation of RASSF1A.
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publishDate	2019
allfields	10.1080/15592294.2019.1615355 doi (DE-627)DOAJ098188739 (DE-599)DOAJdaae055f921d4610bf0e3d6d882f360f DE-627 ger DE-627 rakwb eng QH426-470 Naiade Calanca verfasserin aut The long non-coding RNA ANRASSF1 in the regulation of alternative protein-coding transcripts RASSF1A and RASSF1C in human breast cancer cells: implications to epigenetic therapy 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Alternative protein-coding transcripts of the RASSF1 gene have been associated with dual functions in human cancer: while RASSF1C isoform has oncogenic properties, RASSF1A is a tumour suppressor frequently silenced by hypermethylation. Recently, the antisense long non-coding RNA RASSF1 (ANRASSF1) was implicated in a locus-specific mechanism for the RASSF1A epigenetic repression mediated by PRC2 (Polycomb Repressive Complex 2). Here, we evaluated the methylation patterns of the promoter regions of RASSF1A and RASSF1C and the expression levels of these RASSF1 transcripts in breast cancer and breast cancer cell lines. As expected, RASSF1C remained unmethylated and RASSF1A was hypermethylated at high frequencies in 75 primary breast cancers, and also in a panel of three mammary epithelial cells (MEC) and 10 breast cancer cell lines (BCC). Although RASSF1C was expressed in all cell lines, only two of them expressed the transcript RASSF1A. ANRASSF1 expression levels were increased in six BCCs. In vitro induced demethylation with 5-Aza-2ʹ-deoxicytydine (5-Aza-dC) resulted in up-regulation of RASSF1A and an inverse correlation with ANRASSF1 relative abundance in BCCs. However, increased levels of both transcripts were observed in two MECs (184A1 and MCF10A) after treatment with 5-Aza-dC. Overall, these findings indicate that ANRASSF1 is differentially expressed in MECs and BCCs. The lncRNA ANRASSF1 provides new perspectives as a therapeutic target for locus-specific regulation of RASSF1A. dna methylation rassf1a rassf1c rassf1-as1 lncrna locus-specific epigenetic repression Genetics Ana Paula Paschoal verfasserin aut Érika Prando Munhoz verfasserin aut Layla Testa Galindo verfasserin aut Barbara Mitsuyasu Barbosa verfasserin aut José Roberto Fígaro Caldeira verfasserin aut Rogério Antonio Oliveira verfasserin aut Luciane Regina Cavalli verfasserin aut Silvia Regina Rogatto verfasserin aut Cláudia Aparecida Rainho verfasserin aut In Epigenetics Taylor & Francis Group, 2023 14(2019), 8, Seite 741-750 (DE-627)516805320 (DE-600)2248598-3 15592308 nnns volume:14 year:2019 number:8 pages:741-750 https://doi.org/10.1080/15592294.2019.1615355 kostenfrei https://doaj.org/article/daae055f921d4610bf0e3d6d882f360f kostenfrei http://dx.doi.org/10.1080/15592294.2019.1615355 kostenfrei https://doaj.org/toc/1559-2294 Journal toc kostenfrei https://doaj.org/toc/1559-2308 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_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_211 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_647 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2026 GBV_ILN_2034 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2111 GBV_ILN_2129 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4046 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_4393 GBV_ILN_4700 AR 14 2019 8 741-750
spelling	10.1080/15592294.2019.1615355 doi (DE-627)DOAJ098188739 (DE-599)DOAJdaae055f921d4610bf0e3d6d882f360f DE-627 ger DE-627 rakwb eng QH426-470 Naiade Calanca verfasserin aut The long non-coding RNA ANRASSF1 in the regulation of alternative protein-coding transcripts RASSF1A and RASSF1C in human breast cancer cells: implications to epigenetic therapy 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Alternative protein-coding transcripts of the RASSF1 gene have been associated with dual functions in human cancer: while RASSF1C isoform has oncogenic properties, RASSF1A is a tumour suppressor frequently silenced by hypermethylation. Recently, the antisense long non-coding RNA RASSF1 (ANRASSF1) was implicated in a locus-specific mechanism for the RASSF1A epigenetic repression mediated by PRC2 (Polycomb Repressive Complex 2). Here, we evaluated the methylation patterns of the promoter regions of RASSF1A and RASSF1C and the expression levels of these RASSF1 transcripts in breast cancer and breast cancer cell lines. As expected, RASSF1C remained unmethylated and RASSF1A was hypermethylated at high frequencies in 75 primary breast cancers, and also in a panel of three mammary epithelial cells (MEC) and 10 breast cancer cell lines (BCC). Although RASSF1C was expressed in all cell lines, only two of them expressed the transcript RASSF1A. ANRASSF1 expression levels were increased in six BCCs. In vitro induced demethylation with 5-Aza-2ʹ-deoxicytydine (5-Aza-dC) resulted in up-regulation of RASSF1A and an inverse correlation with ANRASSF1 relative abundance in BCCs. However, increased levels of both transcripts were observed in two MECs (184A1 and MCF10A) after treatment with 5-Aza-dC. Overall, these findings indicate that ANRASSF1 is differentially expressed in MECs and BCCs. The lncRNA ANRASSF1 provides new perspectives as a therapeutic target for locus-specific regulation of RASSF1A. dna methylation rassf1a rassf1c rassf1-as1 lncrna locus-specific epigenetic repression Genetics Ana Paula Paschoal verfasserin aut Érika Prando Munhoz verfasserin aut Layla Testa Galindo verfasserin aut Barbara Mitsuyasu Barbosa verfasserin aut José Roberto Fígaro Caldeira verfasserin aut Rogério Antonio Oliveira verfasserin aut Luciane Regina Cavalli verfasserin aut Silvia Regina Rogatto verfasserin aut Cláudia Aparecida Rainho verfasserin aut In Epigenetics Taylor & Francis Group, 2023 14(2019), 8, Seite 741-750 (DE-627)516805320 (DE-600)2248598-3 15592308 nnns volume:14 year:2019 number:8 pages:741-750 https://doi.org/10.1080/15592294.2019.1615355 kostenfrei https://doaj.org/article/daae055f921d4610bf0e3d6d882f360f kostenfrei http://dx.doi.org/10.1080/15592294.2019.1615355 kostenfrei https://doaj.org/toc/1559-2294 Journal toc kostenfrei https://doaj.org/toc/1559-2308 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_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_211 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_647 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2026 GBV_ILN_2034 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2111 GBV_ILN_2129 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4046 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_4393 GBV_ILN_4700 AR 14 2019 8 741-750
allfields_unstemmed	10.1080/15592294.2019.1615355 doi (DE-627)DOAJ098188739 (DE-599)DOAJdaae055f921d4610bf0e3d6d882f360f DE-627 ger DE-627 rakwb eng QH426-470 Naiade Calanca verfasserin aut The long non-coding RNA ANRASSF1 in the regulation of alternative protein-coding transcripts RASSF1A and RASSF1C in human breast cancer cells: implications to epigenetic therapy 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Alternative protein-coding transcripts of the RASSF1 gene have been associated with dual functions in human cancer: while RASSF1C isoform has oncogenic properties, RASSF1A is a tumour suppressor frequently silenced by hypermethylation. Recently, the antisense long non-coding RNA RASSF1 (ANRASSF1) was implicated in a locus-specific mechanism for the RASSF1A epigenetic repression mediated by PRC2 (Polycomb Repressive Complex 2). Here, we evaluated the methylation patterns of the promoter regions of RASSF1A and RASSF1C and the expression levels of these RASSF1 transcripts in breast cancer and breast cancer cell lines. As expected, RASSF1C remained unmethylated and RASSF1A was hypermethylated at high frequencies in 75 primary breast cancers, and also in a panel of three mammary epithelial cells (MEC) and 10 breast cancer cell lines (BCC). Although RASSF1C was expressed in all cell lines, only two of them expressed the transcript RASSF1A. ANRASSF1 expression levels were increased in six BCCs. In vitro induced demethylation with 5-Aza-2ʹ-deoxicytydine (5-Aza-dC) resulted in up-regulation of RASSF1A and an inverse correlation with ANRASSF1 relative abundance in BCCs. However, increased levels of both transcripts were observed in two MECs (184A1 and MCF10A) after treatment with 5-Aza-dC. Overall, these findings indicate that ANRASSF1 is differentially expressed in MECs and BCCs. The lncRNA ANRASSF1 provides new perspectives as a therapeutic target for locus-specific regulation of RASSF1A. dna methylation rassf1a rassf1c rassf1-as1 lncrna locus-specific epigenetic repression Genetics Ana Paula Paschoal verfasserin aut Érika Prando Munhoz verfasserin aut Layla Testa Galindo verfasserin aut Barbara Mitsuyasu Barbosa verfasserin aut José Roberto Fígaro Caldeira verfasserin aut Rogério Antonio Oliveira verfasserin aut Luciane Regina Cavalli verfasserin aut Silvia Regina Rogatto verfasserin aut Cláudia Aparecida Rainho verfasserin aut In Epigenetics Taylor & Francis Group, 2023 14(2019), 8, Seite 741-750 (DE-627)516805320 (DE-600)2248598-3 15592308 nnns volume:14 year:2019 number:8 pages:741-750 https://doi.org/10.1080/15592294.2019.1615355 kostenfrei https://doaj.org/article/daae055f921d4610bf0e3d6d882f360f kostenfrei http://dx.doi.org/10.1080/15592294.2019.1615355 kostenfrei https://doaj.org/toc/1559-2294 Journal toc kostenfrei https://doaj.org/toc/1559-2308 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_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_211 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_647 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2026 GBV_ILN_2034 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2111 GBV_ILN_2129 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4046 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_4393 GBV_ILN_4700 AR 14 2019 8 741-750
allfieldsGer	10.1080/15592294.2019.1615355 doi (DE-627)DOAJ098188739 (DE-599)DOAJdaae055f921d4610bf0e3d6d882f360f DE-627 ger DE-627 rakwb eng QH426-470 Naiade Calanca verfasserin aut The long non-coding RNA ANRASSF1 in the regulation of alternative protein-coding transcripts RASSF1A and RASSF1C in human breast cancer cells: implications to epigenetic therapy 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Alternative protein-coding transcripts of the RASSF1 gene have been associated with dual functions in human cancer: while RASSF1C isoform has oncogenic properties, RASSF1A is a tumour suppressor frequently silenced by hypermethylation. Recently, the antisense long non-coding RNA RASSF1 (ANRASSF1) was implicated in a locus-specific mechanism for the RASSF1A epigenetic repression mediated by PRC2 (Polycomb Repressive Complex 2). Here, we evaluated the methylation patterns of the promoter regions of RASSF1A and RASSF1C and the expression levels of these RASSF1 transcripts in breast cancer and breast cancer cell lines. As expected, RASSF1C remained unmethylated and RASSF1A was hypermethylated at high frequencies in 75 primary breast cancers, and also in a panel of three mammary epithelial cells (MEC) and 10 breast cancer cell lines (BCC). Although RASSF1C was expressed in all cell lines, only two of them expressed the transcript RASSF1A. ANRASSF1 expression levels were increased in six BCCs. In vitro induced demethylation with 5-Aza-2ʹ-deoxicytydine (5-Aza-dC) resulted in up-regulation of RASSF1A and an inverse correlation with ANRASSF1 relative abundance in BCCs. However, increased levels of both transcripts were observed in two MECs (184A1 and MCF10A) after treatment with 5-Aza-dC. Overall, these findings indicate that ANRASSF1 is differentially expressed in MECs and BCCs. The lncRNA ANRASSF1 provides new perspectives as a therapeutic target for locus-specific regulation of RASSF1A. dna methylation rassf1a rassf1c rassf1-as1 lncrna locus-specific epigenetic repression Genetics Ana Paula Paschoal verfasserin aut Érika Prando Munhoz verfasserin aut Layla Testa Galindo verfasserin aut Barbara Mitsuyasu Barbosa verfasserin aut José Roberto Fígaro Caldeira verfasserin aut Rogério Antonio Oliveira verfasserin aut Luciane Regina Cavalli verfasserin aut Silvia Regina Rogatto verfasserin aut Cláudia Aparecida Rainho verfasserin aut In Epigenetics Taylor & Francis Group, 2023 14(2019), 8, Seite 741-750 (DE-627)516805320 (DE-600)2248598-3 15592308 nnns volume:14 year:2019 number:8 pages:741-750 https://doi.org/10.1080/15592294.2019.1615355 kostenfrei https://doaj.org/article/daae055f921d4610bf0e3d6d882f360f kostenfrei http://dx.doi.org/10.1080/15592294.2019.1615355 kostenfrei https://doaj.org/toc/1559-2294 Journal toc kostenfrei https://doaj.org/toc/1559-2308 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_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_211 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_647 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2026 GBV_ILN_2034 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2111 GBV_ILN_2129 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4046 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_4393 GBV_ILN_4700 AR 14 2019 8 741-750
allfieldsSound	10.1080/15592294.2019.1615355 doi (DE-627)DOAJ098188739 (DE-599)DOAJdaae055f921d4610bf0e3d6d882f360f DE-627 ger DE-627 rakwb eng QH426-470 Naiade Calanca verfasserin aut The long non-coding RNA ANRASSF1 in the regulation of alternative protein-coding transcripts RASSF1A and RASSF1C in human breast cancer cells: implications to epigenetic therapy 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Alternative protein-coding transcripts of the RASSF1 gene have been associated with dual functions in human cancer: while RASSF1C isoform has oncogenic properties, RASSF1A is a tumour suppressor frequently silenced by hypermethylation. Recently, the antisense long non-coding RNA RASSF1 (ANRASSF1) was implicated in a locus-specific mechanism for the RASSF1A epigenetic repression mediated by PRC2 (Polycomb Repressive Complex 2). Here, we evaluated the methylation patterns of the promoter regions of RASSF1A and RASSF1C and the expression levels of these RASSF1 transcripts in breast cancer and breast cancer cell lines. As expected, RASSF1C remained unmethylated and RASSF1A was hypermethylated at high frequencies in 75 primary breast cancers, and also in a panel of three mammary epithelial cells (MEC) and 10 breast cancer cell lines (BCC). Although RASSF1C was expressed in all cell lines, only two of them expressed the transcript RASSF1A. ANRASSF1 expression levels were increased in six BCCs. In vitro induced demethylation with 5-Aza-2ʹ-deoxicytydine (5-Aza-dC) resulted in up-regulation of RASSF1A and an inverse correlation with ANRASSF1 relative abundance in BCCs. However, increased levels of both transcripts were observed in two MECs (184A1 and MCF10A) after treatment with 5-Aza-dC. Overall, these findings indicate that ANRASSF1 is differentially expressed in MECs and BCCs. The lncRNA ANRASSF1 provides new perspectives as a therapeutic target for locus-specific regulation of RASSF1A. dna methylation rassf1a rassf1c rassf1-as1 lncrna locus-specific epigenetic repression Genetics Ana Paula Paschoal verfasserin aut Érika Prando Munhoz verfasserin aut Layla Testa Galindo verfasserin aut Barbara Mitsuyasu Barbosa verfasserin aut José Roberto Fígaro Caldeira verfasserin aut Rogério Antonio Oliveira verfasserin aut Luciane Regina Cavalli verfasserin aut Silvia Regina Rogatto verfasserin aut Cláudia Aparecida Rainho verfasserin aut In Epigenetics Taylor & Francis Group, 2023 14(2019), 8, Seite 741-750 (DE-627)516805320 (DE-600)2248598-3 15592308 nnns volume:14 year:2019 number:8 pages:741-750 https://doi.org/10.1080/15592294.2019.1615355 kostenfrei https://doaj.org/article/daae055f921d4610bf0e3d6d882f360f kostenfrei http://dx.doi.org/10.1080/15592294.2019.1615355 kostenfrei https://doaj.org/toc/1559-2294 Journal toc kostenfrei https://doaj.org/toc/1559-2308 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_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_211 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_647 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2026 GBV_ILN_2034 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2111 GBV_ILN_2129 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4046 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_4393 GBV_ILN_4700 AR 14 2019 8 741-750
language	English
source	In Epigenetics 14(2019), 8, Seite 741-750 volume:14 year:2019 number:8 pages:741-750
sourceStr	In Epigenetics 14(2019), 8, Seite 741-750 volume:14 year:2019 number:8 pages:741-750
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	dna methylation rassf1a rassf1c rassf1-as1 lncrna locus-specific epigenetic repression Genetics
isfreeaccess_bool	true
container_title	Epigenetics
authorswithroles_txt_mv	Naiade Calanca @@aut@@ Ana Paula Paschoal @@aut@@ Érika Prando Munhoz @@aut@@ Layla Testa Galindo @@aut@@ Barbara Mitsuyasu Barbosa @@aut@@ José Roberto Fígaro Caldeira @@aut@@ Rogério Antonio Oliveira @@aut@@ Luciane Regina Cavalli @@aut@@ Silvia Regina Rogatto @@aut@@ Cláudia Aparecida Rainho @@aut@@
publishDateDaySort_date	2019-01-01T00:00:00Z
hierarchy_top_id	516805320
id	DOAJ098188739
language_de	englisch
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callnumber-first	Q - Science
author	Naiade Calanca
spellingShingle	Naiade Calanca misc QH426-470 misc dna methylation misc rassf1a misc rassf1c misc rassf1-as1 misc lncrna misc locus-specific epigenetic repression misc Genetics The long non-coding RNA ANRASSF1 in the regulation of alternative protein-coding transcripts RASSF1A and RASSF1C in human breast cancer cells: implications to epigenetic therapy
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topic_title	QH426-470 The long non-coding RNA ANRASSF1 in the regulation of alternative protein-coding transcripts RASSF1A and RASSF1C in human breast cancer cells: implications to epigenetic therapy dna methylation rassf1a rassf1c rassf1-as1 lncrna locus-specific epigenetic repression
topic	misc QH426-470 misc dna methylation misc rassf1a misc rassf1c misc rassf1-as1 misc lncrna misc locus-specific epigenetic repression misc Genetics
topic_unstemmed	misc QH426-470 misc dna methylation misc rassf1a misc rassf1c misc rassf1-as1 misc lncrna misc locus-specific epigenetic repression misc Genetics
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title	The long non-coding RNA ANRASSF1 in the regulation of alternative protein-coding transcripts RASSF1A and RASSF1C in human breast cancer cells: implications to epigenetic therapy
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title_full	The long non-coding RNA ANRASSF1 in the regulation of alternative protein-coding transcripts RASSF1A and RASSF1C in human breast cancer cells: implications to epigenetic therapy
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title_sort	long non-coding rna anrassf1 in the regulation of alternative protein-coding transcripts rassf1a and rassf1c in human breast cancer cells: implications to epigenetic therapy
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title_auth	The long non-coding RNA ANRASSF1 in the regulation of alternative protein-coding transcripts RASSF1A and RASSF1C in human breast cancer cells: implications to epigenetic therapy
abstract	Alternative protein-coding transcripts of the RASSF1 gene have been associated with dual functions in human cancer: while RASSF1C isoform has oncogenic properties, RASSF1A is a tumour suppressor frequently silenced by hypermethylation. Recently, the antisense long non-coding RNA RASSF1 (ANRASSF1) was implicated in a locus-specific mechanism for the RASSF1A epigenetic repression mediated by PRC2 (Polycomb Repressive Complex 2). Here, we evaluated the methylation patterns of the promoter regions of RASSF1A and RASSF1C and the expression levels of these RASSF1 transcripts in breast cancer and breast cancer cell lines. As expected, RASSF1C remained unmethylated and RASSF1A was hypermethylated at high frequencies in 75 primary breast cancers, and also in a panel of three mammary epithelial cells (MEC) and 10 breast cancer cell lines (BCC). Although RASSF1C was expressed in all cell lines, only two of them expressed the transcript RASSF1A. ANRASSF1 expression levels were increased in six BCCs. In vitro induced demethylation with 5-Aza-2ʹ-deoxicytydine (5-Aza-dC) resulted in up-regulation of RASSF1A and an inverse correlation with ANRASSF1 relative abundance in BCCs. However, increased levels of both transcripts were observed in two MECs (184A1 and MCF10A) after treatment with 5-Aza-dC. Overall, these findings indicate that ANRASSF1 is differentially expressed in MECs and BCCs. The lncRNA ANRASSF1 provides new perspectives as a therapeutic target for locus-specific regulation of RASSF1A.
abstractGer	Alternative protein-coding transcripts of the RASSF1 gene have been associated with dual functions in human cancer: while RASSF1C isoform has oncogenic properties, RASSF1A is a tumour suppressor frequently silenced by hypermethylation. Recently, the antisense long non-coding RNA RASSF1 (ANRASSF1) was implicated in a locus-specific mechanism for the RASSF1A epigenetic repression mediated by PRC2 (Polycomb Repressive Complex 2). Here, we evaluated the methylation patterns of the promoter regions of RASSF1A and RASSF1C and the expression levels of these RASSF1 transcripts in breast cancer and breast cancer cell lines. As expected, RASSF1C remained unmethylated and RASSF1A was hypermethylated at high frequencies in 75 primary breast cancers, and also in a panel of three mammary epithelial cells (MEC) and 10 breast cancer cell lines (BCC). Although RASSF1C was expressed in all cell lines, only two of them expressed the transcript RASSF1A. ANRASSF1 expression levels were increased in six BCCs. In vitro induced demethylation with 5-Aza-2ʹ-deoxicytydine (5-Aza-dC) resulted in up-regulation of RASSF1A and an inverse correlation with ANRASSF1 relative abundance in BCCs. However, increased levels of both transcripts were observed in two MECs (184A1 and MCF10A) after treatment with 5-Aza-dC. Overall, these findings indicate that ANRASSF1 is differentially expressed in MECs and BCCs. The lncRNA ANRASSF1 provides new perspectives as a therapeutic target for locus-specific regulation of RASSF1A.
abstract_unstemmed	Alternative protein-coding transcripts of the RASSF1 gene have been associated with dual functions in human cancer: while RASSF1C isoform has oncogenic properties, RASSF1A is a tumour suppressor frequently silenced by hypermethylation. Recently, the antisense long non-coding RNA RASSF1 (ANRASSF1) was implicated in a locus-specific mechanism for the RASSF1A epigenetic repression mediated by PRC2 (Polycomb Repressive Complex 2). Here, we evaluated the methylation patterns of the promoter regions of RASSF1A and RASSF1C and the expression levels of these RASSF1 transcripts in breast cancer and breast cancer cell lines. As expected, RASSF1C remained unmethylated and RASSF1A was hypermethylated at high frequencies in 75 primary breast cancers, and also in a panel of three mammary epithelial cells (MEC) and 10 breast cancer cell lines (BCC). Although RASSF1C was expressed in all cell lines, only two of them expressed the transcript RASSF1A. ANRASSF1 expression levels were increased in six BCCs. In vitro induced demethylation with 5-Aza-2ʹ-deoxicytydine (5-Aza-dC) resulted in up-regulation of RASSF1A and an inverse correlation with ANRASSF1 relative abundance in BCCs. However, increased levels of both transcripts were observed in two MECs (184A1 and MCF10A) after treatment with 5-Aza-dC. Overall, these findings indicate that ANRASSF1 is differentially expressed in MECs and BCCs. The lncRNA ANRASSF1 provides new perspectives as a therapeutic target for locus-specific regulation of RASSF1A.
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title_short	The long non-coding RNA ANRASSF1 in the regulation of alternative protein-coding transcripts RASSF1A and RASSF1C in human breast cancer cells: implications to epigenetic therapy
url	https://doi.org/10.1080/15592294.2019.1615355 https://doaj.org/article/daae055f921d4610bf0e3d6d882f360f http://dx.doi.org/10.1080/15592294.2019.1615355 https://doaj.org/toc/1559-2294 https://doaj.org/toc/1559-2308
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Recently, the antisense long non-coding RNA RASSF1 (ANRASSF1) was implicated in a locus-specific mechanism for the RASSF1A epigenetic repression mediated by PRC2 (Polycomb Repressive Complex 2). Here, we evaluated the methylation patterns of the promoter regions of RASSF1A and RASSF1C and the expression levels of these RASSF1 transcripts in breast cancer and breast cancer cell lines. As expected, RASSF1C remained unmethylated and RASSF1A was hypermethylated at high frequencies in 75 primary breast cancers, and also in a panel of three mammary epithelial cells (MEC) and 10 breast cancer cell lines (BCC). Although RASSF1C was expressed in all cell lines, only two of them expressed the transcript RASSF1A. ANRASSF1 expression levels were increased in six BCCs. In vitro induced demethylation with 5-Aza-2ʹ-deoxicytydine (5-Aza-dC) resulted in up-regulation of RASSF1A and an inverse correlation with ANRASSF1 relative abundance in BCCs. However, increased levels of both transcripts were observed in two MECs (184A1 and MCF10A) after treatment with 5-Aza-dC. Overall, these findings indicate that ANRASSF1 is differentially expressed in MECs and BCCs. 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The long non-coding RNA ANRASSF1 in the regulation of alternative protein-coding transcripts RASSF1A and RASSF1C in human breast cancer cells: implications to epigenetic therapy

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