TRPS1 drives heterochromatic origin refiring and cancer genome evolution

Summary: Exploitation of naturally occurring genetic mutations could empower the discovery of novel aspects of established cancer genes. We report here that TRPS1, a gene linked to the tricho-rhino-phalangeal syndrome (TRPS) and recently identified as a potential breast cancer driver, promotes breas...
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Autor*in:	Jianguo Yang [verfasserIn] Xiaoping Liu [verfasserIn] Yunchao Huang [verfasserIn] Lin He [verfasserIn] Wenting Zhang [verfasserIn] Jie Ren [verfasserIn] Yue Wang [verfasserIn] Jiajing Wu [verfasserIn] Xiaodi Wu [verfasserIn] Lin Shan [verfasserIn] Xiaohan Yang [verfasserIn] Luyang Sun [verfasserIn] Jing Liang [verfasserIn] Yu Zhang [verfasserIn] Yongfeng Shang [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2021

Schlagwörter:	heterochromatic origin refiring TRPS1 H3K9me3 breast cancer cancer genome evolution therapeutic resistance

Übergeordnetes Werk:	In: Cell Reports - Elsevier, 2015, 34(2021), 10, Seite 108814-
Übergeordnetes Werk:	volume:34 ; year:2021 ; number:10 ; pages:108814-

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1016/j.celrep.2021.108814

Katalog-ID:	DOAJ006793843

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520			\|a Summary: Exploitation of naturally occurring genetic mutations could empower the discovery of novel aspects of established cancer genes. We report here that TRPS1, a gene linked to the tricho-rhino-phalangeal syndrome (TRPS) and recently identified as a potential breast cancer driver, promotes breast carcinogenesis through regulating replication. Epigenomic decomposition of TRPS1 landscape reveals nearly half of H3K9me3-marked heterochromatic origins are occupied by TRPS1, where it encourages the chromatin loading of APC/C, resulting in uncontrolled origin refiring. TRPS1 binds to the genome through its atypical H3K9me3 reading via GATA and IKAROS domains, while TRPS-related mutations affect its chromatin binding, replication boosting, and tumorigenicity. Concordantly, overexpression of wild-type but not TRPS-associated mutants of TRPS1 is sufficient to drive cancer genome amplifications, which experience an extrachromosomal route and dynamically evolve to confer therapeutic resistance. Together, these results uncover a critical function of TRPS1 in driving heterochromatin origin firing and breast cancer genome evolution.
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allfields	10.1016/j.celrep.2021.108814 doi (DE-627)DOAJ006793843 (DE-599)DOAJb658d630f0974c88869c1af9df9bf455 DE-627 ger DE-627 rakwb eng QH301-705.5 Jianguo Yang verfasserin aut TRPS1 drives heterochromatic origin refiring and cancer genome evolution 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary: Exploitation of naturally occurring genetic mutations could empower the discovery of novel aspects of established cancer genes. We report here that TRPS1, a gene linked to the tricho-rhino-phalangeal syndrome (TRPS) and recently identified as a potential breast cancer driver, promotes breast carcinogenesis through regulating replication. Epigenomic decomposition of TRPS1 landscape reveals nearly half of H3K9me3-marked heterochromatic origins are occupied by TRPS1, where it encourages the chromatin loading of APC/C, resulting in uncontrolled origin refiring. TRPS1 binds to the genome through its atypical H3K9me3 reading via GATA and IKAROS domains, while TRPS-related mutations affect its chromatin binding, replication boosting, and tumorigenicity. Concordantly, overexpression of wild-type but not TRPS-associated mutants of TRPS1 is sufficient to drive cancer genome amplifications, which experience an extrachromosomal route and dynamically evolve to confer therapeutic resistance. Together, these results uncover a critical function of TRPS1 in driving heterochromatin origin firing and breast cancer genome evolution. heterochromatic origin refiring TRPS1 H3K9me3 breast cancer cancer genome evolution therapeutic resistance Biology (General) Xiaoping Liu verfasserin aut Yunchao Huang verfasserin aut Lin He verfasserin aut Wenting Zhang verfasserin aut Jie Ren verfasserin aut Yue Wang verfasserin aut Jiajing Wu verfasserin aut Xiaodi Wu verfasserin aut Lin Shan verfasserin aut Xiaohan Yang verfasserin aut Luyang Sun verfasserin aut Jing Liang verfasserin aut Yu Zhang verfasserin aut Yongfeng Shang verfasserin aut In Cell Reports Elsevier, 2015 34(2021), 10, Seite 108814- (DE-627)684964562 (DE-600)2649101-1 22111247 nnns volume:34 year:2021 number:10 pages:108814- https://doi.org/10.1016/j.celrep.2021.108814 kostenfrei https://doaj.org/article/b658d630f0974c88869c1af9df9bf455 kostenfrei http://www.sciencedirect.com/science/article/pii/S2211124721001285 kostenfrei https://doaj.org/toc/2211-1247 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 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_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 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_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 34 2021 10 108814-
spelling	10.1016/j.celrep.2021.108814 doi (DE-627)DOAJ006793843 (DE-599)DOAJb658d630f0974c88869c1af9df9bf455 DE-627 ger DE-627 rakwb eng QH301-705.5 Jianguo Yang verfasserin aut TRPS1 drives heterochromatic origin refiring and cancer genome evolution 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary: Exploitation of naturally occurring genetic mutations could empower the discovery of novel aspects of established cancer genes. We report here that TRPS1, a gene linked to the tricho-rhino-phalangeal syndrome (TRPS) and recently identified as a potential breast cancer driver, promotes breast carcinogenesis through regulating replication. Epigenomic decomposition of TRPS1 landscape reveals nearly half of H3K9me3-marked heterochromatic origins are occupied by TRPS1, where it encourages the chromatin loading of APC/C, resulting in uncontrolled origin refiring. TRPS1 binds to the genome through its atypical H3K9me3 reading via GATA and IKAROS domains, while TRPS-related mutations affect its chromatin binding, replication boosting, and tumorigenicity. Concordantly, overexpression of wild-type but not TRPS-associated mutants of TRPS1 is sufficient to drive cancer genome amplifications, which experience an extrachromosomal route and dynamically evolve to confer therapeutic resistance. Together, these results uncover a critical function of TRPS1 in driving heterochromatin origin firing and breast cancer genome evolution. heterochromatic origin refiring TRPS1 H3K9me3 breast cancer cancer genome evolution therapeutic resistance Biology (General) Xiaoping Liu verfasserin aut Yunchao Huang verfasserin aut Lin He verfasserin aut Wenting Zhang verfasserin aut Jie Ren verfasserin aut Yue Wang verfasserin aut Jiajing Wu verfasserin aut Xiaodi Wu verfasserin aut Lin Shan verfasserin aut Xiaohan Yang verfasserin aut Luyang Sun verfasserin aut Jing Liang verfasserin aut Yu Zhang verfasserin aut Yongfeng Shang verfasserin aut In Cell Reports Elsevier, 2015 34(2021), 10, Seite 108814- (DE-627)684964562 (DE-600)2649101-1 22111247 nnns volume:34 year:2021 number:10 pages:108814- https://doi.org/10.1016/j.celrep.2021.108814 kostenfrei https://doaj.org/article/b658d630f0974c88869c1af9df9bf455 kostenfrei http://www.sciencedirect.com/science/article/pii/S2211124721001285 kostenfrei https://doaj.org/toc/2211-1247 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 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_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 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_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 34 2021 10 108814-
allfields_unstemmed	10.1016/j.celrep.2021.108814 doi (DE-627)DOAJ006793843 (DE-599)DOAJb658d630f0974c88869c1af9df9bf455 DE-627 ger DE-627 rakwb eng QH301-705.5 Jianguo Yang verfasserin aut TRPS1 drives heterochromatic origin refiring and cancer genome evolution 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary: Exploitation of naturally occurring genetic mutations could empower the discovery of novel aspects of established cancer genes. We report here that TRPS1, a gene linked to the tricho-rhino-phalangeal syndrome (TRPS) and recently identified as a potential breast cancer driver, promotes breast carcinogenesis through regulating replication. Epigenomic decomposition of TRPS1 landscape reveals nearly half of H3K9me3-marked heterochromatic origins are occupied by TRPS1, where it encourages the chromatin loading of APC/C, resulting in uncontrolled origin refiring. TRPS1 binds to the genome through its atypical H3K9me3 reading via GATA and IKAROS domains, while TRPS-related mutations affect its chromatin binding, replication boosting, and tumorigenicity. Concordantly, overexpression of wild-type but not TRPS-associated mutants of TRPS1 is sufficient to drive cancer genome amplifications, which experience an extrachromosomal route and dynamically evolve to confer therapeutic resistance. Together, these results uncover a critical function of TRPS1 in driving heterochromatin origin firing and breast cancer genome evolution. heterochromatic origin refiring TRPS1 H3K9me3 breast cancer cancer genome evolution therapeutic resistance Biology (General) Xiaoping Liu verfasserin aut Yunchao Huang verfasserin aut Lin He verfasserin aut Wenting Zhang verfasserin aut Jie Ren verfasserin aut Yue Wang verfasserin aut Jiajing Wu verfasserin aut Xiaodi Wu verfasserin aut Lin Shan verfasserin aut Xiaohan Yang verfasserin aut Luyang Sun verfasserin aut Jing Liang verfasserin aut Yu Zhang verfasserin aut Yongfeng Shang verfasserin aut In Cell Reports Elsevier, 2015 34(2021), 10, Seite 108814- (DE-627)684964562 (DE-600)2649101-1 22111247 nnns volume:34 year:2021 number:10 pages:108814- https://doi.org/10.1016/j.celrep.2021.108814 kostenfrei https://doaj.org/article/b658d630f0974c88869c1af9df9bf455 kostenfrei http://www.sciencedirect.com/science/article/pii/S2211124721001285 kostenfrei https://doaj.org/toc/2211-1247 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 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_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 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_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 34 2021 10 108814-
allfieldsGer	10.1016/j.celrep.2021.108814 doi (DE-627)DOAJ006793843 (DE-599)DOAJb658d630f0974c88869c1af9df9bf455 DE-627 ger DE-627 rakwb eng QH301-705.5 Jianguo Yang verfasserin aut TRPS1 drives heterochromatic origin refiring and cancer genome evolution 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary: Exploitation of naturally occurring genetic mutations could empower the discovery of novel aspects of established cancer genes. We report here that TRPS1, a gene linked to the tricho-rhino-phalangeal syndrome (TRPS) and recently identified as a potential breast cancer driver, promotes breast carcinogenesis through regulating replication. Epigenomic decomposition of TRPS1 landscape reveals nearly half of H3K9me3-marked heterochromatic origins are occupied by TRPS1, where it encourages the chromatin loading of APC/C, resulting in uncontrolled origin refiring. TRPS1 binds to the genome through its atypical H3K9me3 reading via GATA and IKAROS domains, while TRPS-related mutations affect its chromatin binding, replication boosting, and tumorigenicity. Concordantly, overexpression of wild-type but not TRPS-associated mutants of TRPS1 is sufficient to drive cancer genome amplifications, which experience an extrachromosomal route and dynamically evolve to confer therapeutic resistance. Together, these results uncover a critical function of TRPS1 in driving heterochromatin origin firing and breast cancer genome evolution. heterochromatic origin refiring TRPS1 H3K9me3 breast cancer cancer genome evolution therapeutic resistance Biology (General) Xiaoping Liu verfasserin aut Yunchao Huang verfasserin aut Lin He verfasserin aut Wenting Zhang verfasserin aut Jie Ren verfasserin aut Yue Wang verfasserin aut Jiajing Wu verfasserin aut Xiaodi Wu verfasserin aut Lin Shan verfasserin aut Xiaohan Yang verfasserin aut Luyang Sun verfasserin aut Jing Liang verfasserin aut Yu Zhang verfasserin aut Yongfeng Shang verfasserin aut In Cell Reports Elsevier, 2015 34(2021), 10, Seite 108814- (DE-627)684964562 (DE-600)2649101-1 22111247 nnns volume:34 year:2021 number:10 pages:108814- https://doi.org/10.1016/j.celrep.2021.108814 kostenfrei https://doaj.org/article/b658d630f0974c88869c1af9df9bf455 kostenfrei http://www.sciencedirect.com/science/article/pii/S2211124721001285 kostenfrei https://doaj.org/toc/2211-1247 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 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_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 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_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 34 2021 10 108814-
allfieldsSound	10.1016/j.celrep.2021.108814 doi (DE-627)DOAJ006793843 (DE-599)DOAJb658d630f0974c88869c1af9df9bf455 DE-627 ger DE-627 rakwb eng QH301-705.5 Jianguo Yang verfasserin aut TRPS1 drives heterochromatic origin refiring and cancer genome evolution 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary: Exploitation of naturally occurring genetic mutations could empower the discovery of novel aspects of established cancer genes. We report here that TRPS1, a gene linked to the tricho-rhino-phalangeal syndrome (TRPS) and recently identified as a potential breast cancer driver, promotes breast carcinogenesis through regulating replication. Epigenomic decomposition of TRPS1 landscape reveals nearly half of H3K9me3-marked heterochromatic origins are occupied by TRPS1, where it encourages the chromatin loading of APC/C, resulting in uncontrolled origin refiring. TRPS1 binds to the genome through its atypical H3K9me3 reading via GATA and IKAROS domains, while TRPS-related mutations affect its chromatin binding, replication boosting, and tumorigenicity. Concordantly, overexpression of wild-type but not TRPS-associated mutants of TRPS1 is sufficient to drive cancer genome amplifications, which experience an extrachromosomal route and dynamically evolve to confer therapeutic resistance. Together, these results uncover a critical function of TRPS1 in driving heterochromatin origin firing and breast cancer genome evolution. heterochromatic origin refiring TRPS1 H3K9me3 breast cancer cancer genome evolution therapeutic resistance Biology (General) Xiaoping Liu verfasserin aut Yunchao Huang verfasserin aut Lin He verfasserin aut Wenting Zhang verfasserin aut Jie Ren verfasserin aut Yue Wang verfasserin aut Jiajing Wu verfasserin aut Xiaodi Wu verfasserin aut Lin Shan verfasserin aut Xiaohan Yang verfasserin aut Luyang Sun verfasserin aut Jing Liang verfasserin aut Yu Zhang verfasserin aut Yongfeng Shang verfasserin aut In Cell Reports Elsevier, 2015 34(2021), 10, Seite 108814- (DE-627)684964562 (DE-600)2649101-1 22111247 nnns volume:34 year:2021 number:10 pages:108814- https://doi.org/10.1016/j.celrep.2021.108814 kostenfrei https://doaj.org/article/b658d630f0974c88869c1af9df9bf455 kostenfrei http://www.sciencedirect.com/science/article/pii/S2211124721001285 kostenfrei https://doaj.org/toc/2211-1247 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 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_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 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_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 34 2021 10 108814-
language	English
source	In Cell Reports 34(2021), 10, Seite 108814- volume:34 year:2021 number:10 pages:108814-
sourceStr	In Cell Reports 34(2021), 10, Seite 108814- volume:34 year:2021 number:10 pages:108814-
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	heterochromatic origin refiring TRPS1 H3K9me3 breast cancer cancer genome evolution therapeutic resistance Biology (General)
isfreeaccess_bool	true
container_title	Cell Reports
authorswithroles_txt_mv	Jianguo Yang @@aut@@ Xiaoping Liu @@aut@@ Yunchao Huang @@aut@@ Lin He @@aut@@ Wenting Zhang @@aut@@ Jie Ren @@aut@@ Yue Wang @@aut@@ Jiajing Wu @@aut@@ Xiaodi Wu @@aut@@ Lin Shan @@aut@@ Xiaohan Yang @@aut@@ Luyang Sun @@aut@@ Jing Liang @@aut@@ Yu Zhang @@aut@@ Yongfeng Shang @@aut@@
publishDateDaySort_date	2021-01-01T00:00:00Z
hierarchy_top_id	684964562
id	DOAJ006793843
language_de	englisch
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We report here that TRPS1, a gene linked to the tricho-rhino-phalangeal syndrome (TRPS) and recently identified as a potential breast cancer driver, promotes breast carcinogenesis through regulating replication. Epigenomic decomposition of TRPS1 landscape reveals nearly half of H3K9me3-marked heterochromatic origins are occupied by TRPS1, where it encourages the chromatin loading of APC/C, resulting in uncontrolled origin refiring. TRPS1 binds to the genome through its atypical H3K9me3 reading via GATA and IKAROS domains, while TRPS-related mutations affect its chromatin binding, replication boosting, and tumorigenicity. Concordantly, overexpression of wild-type but not TRPS-associated mutants of TRPS1 is sufficient to drive cancer genome amplifications, which experience an extrachromosomal route and dynamically evolve to confer therapeutic resistance. 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callnumber-first	Q - Science
author	Jianguo Yang
spellingShingle	Jianguo Yang misc QH301-705.5 misc heterochromatic origin refiring misc TRPS1 misc H3K9me3 misc breast cancer misc cancer genome evolution misc therapeutic resistance misc Biology (General) TRPS1 drives heterochromatic origin refiring and cancer genome evolution
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topic_title	QH301-705.5 TRPS1 drives heterochromatic origin refiring and cancer genome evolution heterochromatic origin refiring TRPS1 H3K9me3 breast cancer cancer genome evolution therapeutic resistance
topic	misc QH301-705.5 misc heterochromatic origin refiring misc TRPS1 misc H3K9me3 misc breast cancer misc cancer genome evolution misc therapeutic resistance misc Biology (General)
topic_unstemmed	misc QH301-705.5 misc heterochromatic origin refiring misc TRPS1 misc H3K9me3 misc breast cancer misc cancer genome evolution misc therapeutic resistance misc Biology (General)
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title	TRPS1 drives heterochromatic origin refiring and cancer genome evolution
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title_full	TRPS1 drives heterochromatic origin refiring and cancer genome evolution
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author_browse	Jianguo Yang Xiaoping Liu Yunchao Huang Lin He Wenting Zhang Jie Ren Yue Wang Jiajing Wu Xiaodi Wu Lin Shan Xiaohan Yang Luyang Sun Jing Liang Yu Zhang Yongfeng Shang
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title_sort	trps1 drives heterochromatic origin refiring and cancer genome evolution
callnumber	QH301-705.5
title_auth	TRPS1 drives heterochromatic origin refiring and cancer genome evolution
abstract	Summary: Exploitation of naturally occurring genetic mutations could empower the discovery of novel aspects of established cancer genes. We report here that TRPS1, a gene linked to the tricho-rhino-phalangeal syndrome (TRPS) and recently identified as a potential breast cancer driver, promotes breast carcinogenesis through regulating replication. Epigenomic decomposition of TRPS1 landscape reveals nearly half of H3K9me3-marked heterochromatic origins are occupied by TRPS1, where it encourages the chromatin loading of APC/C, resulting in uncontrolled origin refiring. TRPS1 binds to the genome through its atypical H3K9me3 reading via GATA and IKAROS domains, while TRPS-related mutations affect its chromatin binding, replication boosting, and tumorigenicity. Concordantly, overexpression of wild-type but not TRPS-associated mutants of TRPS1 is sufficient to drive cancer genome amplifications, which experience an extrachromosomal route and dynamically evolve to confer therapeutic resistance. Together, these results uncover a critical function of TRPS1 in driving heterochromatin origin firing and breast cancer genome evolution.
abstractGer	Summary: Exploitation of naturally occurring genetic mutations could empower the discovery of novel aspects of established cancer genes. We report here that TRPS1, a gene linked to the tricho-rhino-phalangeal syndrome (TRPS) and recently identified as a potential breast cancer driver, promotes breast carcinogenesis through regulating replication. Epigenomic decomposition of TRPS1 landscape reveals nearly half of H3K9me3-marked heterochromatic origins are occupied by TRPS1, where it encourages the chromatin loading of APC/C, resulting in uncontrolled origin refiring. TRPS1 binds to the genome through its atypical H3K9me3 reading via GATA and IKAROS domains, while TRPS-related mutations affect its chromatin binding, replication boosting, and tumorigenicity. Concordantly, overexpression of wild-type but not TRPS-associated mutants of TRPS1 is sufficient to drive cancer genome amplifications, which experience an extrachromosomal route and dynamically evolve to confer therapeutic resistance. Together, these results uncover a critical function of TRPS1 in driving heterochromatin origin firing and breast cancer genome evolution.
abstract_unstemmed	Summary: Exploitation of naturally occurring genetic mutations could empower the discovery of novel aspects of established cancer genes. We report here that TRPS1, a gene linked to the tricho-rhino-phalangeal syndrome (TRPS) and recently identified as a potential breast cancer driver, promotes breast carcinogenesis through regulating replication. Epigenomic decomposition of TRPS1 landscape reveals nearly half of H3K9me3-marked heterochromatic origins are occupied by TRPS1, where it encourages the chromatin loading of APC/C, resulting in uncontrolled origin refiring. TRPS1 binds to the genome through its atypical H3K9me3 reading via GATA and IKAROS domains, while TRPS-related mutations affect its chromatin binding, replication boosting, and tumorigenicity. Concordantly, overexpression of wild-type but not TRPS-associated mutants of TRPS1 is sufficient to drive cancer genome amplifications, which experience an extrachromosomal route and dynamically evolve to confer therapeutic resistance. Together, these results uncover a critical function of TRPS1 in driving heterochromatin origin firing and breast cancer genome evolution.
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title_short	TRPS1 drives heterochromatic origin refiring and cancer genome evolution
url	https://doi.org/10.1016/j.celrep.2021.108814 https://doaj.org/article/b658d630f0974c88869c1af9df9bf455 http://www.sciencedirect.com/science/article/pii/S2211124721001285 https://doaj.org/toc/2211-1247
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We report here that TRPS1, a gene linked to the tricho-rhino-phalangeal syndrome (TRPS) and recently identified as a potential breast cancer driver, promotes breast carcinogenesis through regulating replication. Epigenomic decomposition of TRPS1 landscape reveals nearly half of H3K9me3-marked heterochromatic origins are occupied by TRPS1, where it encourages the chromatin loading of APC/C, resulting in uncontrolled origin refiring. TRPS1 binds to the genome through its atypical H3K9me3 reading via GATA and IKAROS domains, while TRPS-related mutations affect its chromatin binding, replication boosting, and tumorigenicity. Concordantly, overexpression of wild-type but not TRPS-associated mutants of TRPS1 is sufficient to drive cancer genome amplifications, which experience an extrachromosomal route and dynamically evolve to confer therapeutic resistance. 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code="4">aut</subfield></datafield><datafield tag="700" ind1="0" ind2=" "><subfield code="a">Yongfeng Shang</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">In</subfield><subfield code="t">Cell Reports</subfield><subfield code="d">Elsevier, 2015</subfield><subfield code="g">34(2021), 10, Seite 108814-</subfield><subfield code="w">(DE-627)684964562</subfield><subfield code="w">(DE-600)2649101-1</subfield><subfield code="x">22111247</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:34</subfield><subfield code="g">year:2021</subfield><subfield code="g">number:10</subfield><subfield code="g">pages:108814-</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.celrep.2021.108814</subfield><subfield code="z">kostenfrei</subfield></datafield><datafield tag="856" 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TRPS1 drives heterochromatic origin refiring and cancer genome evolution

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