An optimized MNK1b aptamer, apMNKQ2, and its potential use as a therapeutic agent in breast cancer

Breast cancer is the most commonly diagnosed and leading cause of cancer death among women worldwide. Mitogen-activated protein kinase-interacting kinases (MNKs) promote the expression of several oncogenic proteins and are overexpressed in several types of cancer. In human cells, there are four isof...
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Autor*in:	C. Pinto-Díez [verfasserIn] R. Ferreras-Martín [verfasserIn] R. Carrión-Marchante [verfasserIn] J.I. Klett-Mingo [verfasserIn] M. García-Hernández [verfasserIn] M.I. Pérez-Morgado [verfasserIn] S. Sacristán [verfasserIn] M. Barragán [verfasserIn] M. Seijo-Vila [verfasserIn] I. Tundidor [verfasserIn] S. Blasco-Benito [verfasserIn] E. Pérez-Gómez [verfasserIn] I. Gómez-Pinto [verfasserIn] C. Sánchez [verfasserIn] C. González [verfasserIn] V.M. González [verfasserIn] M.E. Martín [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2022

Schlagwörter:	MT: Oligonucleotides: Therapies and Applications aptamers anti-tumor drug cancer metastasis MNK

Übergeordnetes Werk:	In: Molecular Therapy: Nucleic Acids - Elsevier, 2013, 30(2022), Seite 553-568
Übergeordnetes Werk:	volume:30 ; year:2022 ; pages:553-568

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1016/j.omtn.2022.11.009

Katalog-ID:	DOAJ086026135

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520			\|a Breast cancer is the most commonly diagnosed and leading cause of cancer death among women worldwide. Mitogen-activated protein kinase-interacting kinases (MNKs) promote the expression of several oncogenic proteins and are overexpressed in several types of cancer. In human cells, there are four isoforms of MNKs. The truncated isoform MNK1b, first described in our laboratory, has a higher basal activity and is constitutively active. Aptamers are emerging in recent years as potential therapeutic agents that show significant advantages over drugs of other nature. We have previously obtained and characterized a highly specific aptamer against MNK1b, named apMNK2F, with a dissociation constant in the nanomolar range, which produces significant inhibition of proliferation, migration, and colony formation in breast cancer cells. Furthermore, its sequence analysis predicted two G-quadruplex structures. In this work, we show the optimization process of the aptamer to reduce its size, improving its stability. The obtained aptamer, named apMNKQ2, is able to inhibit proliferation, colony formation, migration, and invasion in breast cancer cells. In murine models of breast cancer, apMNKQ2 has demonstrated its efficacy in reducing tumor volume and the number of metastases. In conclusion, apMNKQ2 could be used as an anti-tumor drug in the future.
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author_variant	c p d cpd r f m rfm r c m rcm j k m jkm m g h mgh m p m mpm s s ss m b mb m s v msv i t it s b b sbb e p g epg i g p igp c s cs c g cg v g vg m m mm
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allfields	10.1016/j.omtn.2022.11.009 doi (DE-627)DOAJ086026135 (DE-599)DOAJd87a996e039e42de8f35b77109b6aca8 DE-627 ger DE-627 rakwb eng RM1-950 C. Pinto-Díez verfasserin aut An optimized MNK1b aptamer, apMNKQ2, and its potential use as a therapeutic agent in breast cancer 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Breast cancer is the most commonly diagnosed and leading cause of cancer death among women worldwide. Mitogen-activated protein kinase-interacting kinases (MNKs) promote the expression of several oncogenic proteins and are overexpressed in several types of cancer. In human cells, there are four isoforms of MNKs. The truncated isoform MNK1b, first described in our laboratory, has a higher basal activity and is constitutively active. Aptamers are emerging in recent years as potential therapeutic agents that show significant advantages over drugs of other nature. We have previously obtained and characterized a highly specific aptamer against MNK1b, named apMNK2F, with a dissociation constant in the nanomolar range, which produces significant inhibition of proliferation, migration, and colony formation in breast cancer cells. Furthermore, its sequence analysis predicted two G-quadruplex structures. In this work, we show the optimization process of the aptamer to reduce its size, improving its stability. The obtained aptamer, named apMNKQ2, is able to inhibit proliferation, colony formation, migration, and invasion in breast cancer cells. In murine models of breast cancer, apMNKQ2 has demonstrated its efficacy in reducing tumor volume and the number of metastases. In conclusion, apMNKQ2 could be used as an anti-tumor drug in the future. MT: Oligonucleotides: Therapies and Applications aptamers anti-tumor drug cancer metastasis MNK Therapeutics. Pharmacology R. Ferreras-Martín verfasserin aut R. Carrión-Marchante verfasserin aut J.I. Klett-Mingo verfasserin aut M. García-Hernández verfasserin aut M.I. Pérez-Morgado verfasserin aut S. Sacristán verfasserin aut M. Barragán verfasserin aut M. Seijo-Vila verfasserin aut I. Tundidor verfasserin aut S. Blasco-Benito verfasserin aut E. Pérez-Gómez verfasserin aut I. Gómez-Pinto verfasserin aut C. Sánchez verfasserin aut C. González verfasserin aut V.M. González verfasserin aut M.E. Martín verfasserin aut In Molecular Therapy: Nucleic Acids Elsevier, 2013 30(2022), Seite 553-568 (DE-627)718632702 (DE-600)2662631-7 21622531 nnns volume:30 year:2022 pages:553-568 https://doi.org/10.1016/j.omtn.2022.11.009 kostenfrei https://doaj.org/article/d87a996e039e42de8f35b77109b6aca8 kostenfrei http://www.sciencedirect.com/science/article/pii/S2162253122003018 kostenfrei https://doaj.org/toc/2162-2531 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_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_2336 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 30 2022 553-568
spelling	10.1016/j.omtn.2022.11.009 doi (DE-627)DOAJ086026135 (DE-599)DOAJd87a996e039e42de8f35b77109b6aca8 DE-627 ger DE-627 rakwb eng RM1-950 C. Pinto-Díez verfasserin aut An optimized MNK1b aptamer, apMNKQ2, and its potential use as a therapeutic agent in breast cancer 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Breast cancer is the most commonly diagnosed and leading cause of cancer death among women worldwide. Mitogen-activated protein kinase-interacting kinases (MNKs) promote the expression of several oncogenic proteins and are overexpressed in several types of cancer. In human cells, there are four isoforms of MNKs. The truncated isoform MNK1b, first described in our laboratory, has a higher basal activity and is constitutively active. Aptamers are emerging in recent years as potential therapeutic agents that show significant advantages over drugs of other nature. We have previously obtained and characterized a highly specific aptamer against MNK1b, named apMNK2F, with a dissociation constant in the nanomolar range, which produces significant inhibition of proliferation, migration, and colony formation in breast cancer cells. Furthermore, its sequence analysis predicted two G-quadruplex structures. In this work, we show the optimization process of the aptamer to reduce its size, improving its stability. The obtained aptamer, named apMNKQ2, is able to inhibit proliferation, colony formation, migration, and invasion in breast cancer cells. In murine models of breast cancer, apMNKQ2 has demonstrated its efficacy in reducing tumor volume and the number of metastases. In conclusion, apMNKQ2 could be used as an anti-tumor drug in the future. MT: Oligonucleotides: Therapies and Applications aptamers anti-tumor drug cancer metastasis MNK Therapeutics. Pharmacology R. Ferreras-Martín verfasserin aut R. Carrión-Marchante verfasserin aut J.I. Klett-Mingo verfasserin aut M. García-Hernández verfasserin aut M.I. Pérez-Morgado verfasserin aut S. Sacristán verfasserin aut M. Barragán verfasserin aut M. Seijo-Vila verfasserin aut I. Tundidor verfasserin aut S. Blasco-Benito verfasserin aut E. Pérez-Gómez verfasserin aut I. Gómez-Pinto verfasserin aut C. Sánchez verfasserin aut C. González verfasserin aut V.M. González verfasserin aut M.E. Martín verfasserin aut In Molecular Therapy: Nucleic Acids Elsevier, 2013 30(2022), Seite 553-568 (DE-627)718632702 (DE-600)2662631-7 21622531 nnns volume:30 year:2022 pages:553-568 https://doi.org/10.1016/j.omtn.2022.11.009 kostenfrei https://doaj.org/article/d87a996e039e42de8f35b77109b6aca8 kostenfrei http://www.sciencedirect.com/science/article/pii/S2162253122003018 kostenfrei https://doaj.org/toc/2162-2531 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_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_2336 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 30 2022 553-568
allfields_unstemmed	10.1016/j.omtn.2022.11.009 doi (DE-627)DOAJ086026135 (DE-599)DOAJd87a996e039e42de8f35b77109b6aca8 DE-627 ger DE-627 rakwb eng RM1-950 C. Pinto-Díez verfasserin aut An optimized MNK1b aptamer, apMNKQ2, and its potential use as a therapeutic agent in breast cancer 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Breast cancer is the most commonly diagnosed and leading cause of cancer death among women worldwide. Mitogen-activated protein kinase-interacting kinases (MNKs) promote the expression of several oncogenic proteins and are overexpressed in several types of cancer. In human cells, there are four isoforms of MNKs. The truncated isoform MNK1b, first described in our laboratory, has a higher basal activity and is constitutively active. Aptamers are emerging in recent years as potential therapeutic agents that show significant advantages over drugs of other nature. We have previously obtained and characterized a highly specific aptamer against MNK1b, named apMNK2F, with a dissociation constant in the nanomolar range, which produces significant inhibition of proliferation, migration, and colony formation in breast cancer cells. Furthermore, its sequence analysis predicted two G-quadruplex structures. In this work, we show the optimization process of the aptamer to reduce its size, improving its stability. The obtained aptamer, named apMNKQ2, is able to inhibit proliferation, colony formation, migration, and invasion in breast cancer cells. In murine models of breast cancer, apMNKQ2 has demonstrated its efficacy in reducing tumor volume and the number of metastases. In conclusion, apMNKQ2 could be used as an anti-tumor drug in the future. MT: Oligonucleotides: Therapies and Applications aptamers anti-tumor drug cancer metastasis MNK Therapeutics. Pharmacology R. Ferreras-Martín verfasserin aut R. Carrión-Marchante verfasserin aut J.I. Klett-Mingo verfasserin aut M. García-Hernández verfasserin aut M.I. Pérez-Morgado verfasserin aut S. Sacristán verfasserin aut M. Barragán verfasserin aut M. Seijo-Vila verfasserin aut I. Tundidor verfasserin aut S. Blasco-Benito verfasserin aut E. Pérez-Gómez verfasserin aut I. Gómez-Pinto verfasserin aut C. Sánchez verfasserin aut C. González verfasserin aut V.M. González verfasserin aut M.E. Martín verfasserin aut In Molecular Therapy: Nucleic Acids Elsevier, 2013 30(2022), Seite 553-568 (DE-627)718632702 (DE-600)2662631-7 21622531 nnns volume:30 year:2022 pages:553-568 https://doi.org/10.1016/j.omtn.2022.11.009 kostenfrei https://doaj.org/article/d87a996e039e42de8f35b77109b6aca8 kostenfrei http://www.sciencedirect.com/science/article/pii/S2162253122003018 kostenfrei https://doaj.org/toc/2162-2531 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_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_2336 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 30 2022 553-568
allfieldsGer	10.1016/j.omtn.2022.11.009 doi (DE-627)DOAJ086026135 (DE-599)DOAJd87a996e039e42de8f35b77109b6aca8 DE-627 ger DE-627 rakwb eng RM1-950 C. Pinto-Díez verfasserin aut An optimized MNK1b aptamer, apMNKQ2, and its potential use as a therapeutic agent in breast cancer 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Breast cancer is the most commonly diagnosed and leading cause of cancer death among women worldwide. Mitogen-activated protein kinase-interacting kinases (MNKs) promote the expression of several oncogenic proteins and are overexpressed in several types of cancer. In human cells, there are four isoforms of MNKs. The truncated isoform MNK1b, first described in our laboratory, has a higher basal activity and is constitutively active. Aptamers are emerging in recent years as potential therapeutic agents that show significant advantages over drugs of other nature. We have previously obtained and characterized a highly specific aptamer against MNK1b, named apMNK2F, with a dissociation constant in the nanomolar range, which produces significant inhibition of proliferation, migration, and colony formation in breast cancer cells. Furthermore, its sequence analysis predicted two G-quadruplex structures. In this work, we show the optimization process of the aptamer to reduce its size, improving its stability. The obtained aptamer, named apMNKQ2, is able to inhibit proliferation, colony formation, migration, and invasion in breast cancer cells. In murine models of breast cancer, apMNKQ2 has demonstrated its efficacy in reducing tumor volume and the number of metastases. In conclusion, apMNKQ2 could be used as an anti-tumor drug in the future. MT: Oligonucleotides: Therapies and Applications aptamers anti-tumor drug cancer metastasis MNK Therapeutics. Pharmacology R. Ferreras-Martín verfasserin aut R. Carrión-Marchante verfasserin aut J.I. Klett-Mingo verfasserin aut M. García-Hernández verfasserin aut M.I. Pérez-Morgado verfasserin aut S. Sacristán verfasserin aut M. Barragán verfasserin aut M. Seijo-Vila verfasserin aut I. Tundidor verfasserin aut S. Blasco-Benito verfasserin aut E. Pérez-Gómez verfasserin aut I. Gómez-Pinto verfasserin aut C. Sánchez verfasserin aut C. González verfasserin aut V.M. González verfasserin aut M.E. Martín verfasserin aut In Molecular Therapy: Nucleic Acids Elsevier, 2013 30(2022), Seite 553-568 (DE-627)718632702 (DE-600)2662631-7 21622531 nnns volume:30 year:2022 pages:553-568 https://doi.org/10.1016/j.omtn.2022.11.009 kostenfrei https://doaj.org/article/d87a996e039e42de8f35b77109b6aca8 kostenfrei http://www.sciencedirect.com/science/article/pii/S2162253122003018 kostenfrei https://doaj.org/toc/2162-2531 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_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_2336 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 30 2022 553-568
allfieldsSound	10.1016/j.omtn.2022.11.009 doi (DE-627)DOAJ086026135 (DE-599)DOAJd87a996e039e42de8f35b77109b6aca8 DE-627 ger DE-627 rakwb eng RM1-950 C. Pinto-Díez verfasserin aut An optimized MNK1b aptamer, apMNKQ2, and its potential use as a therapeutic agent in breast cancer 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Breast cancer is the most commonly diagnosed and leading cause of cancer death among women worldwide. Mitogen-activated protein kinase-interacting kinases (MNKs) promote the expression of several oncogenic proteins and are overexpressed in several types of cancer. In human cells, there are four isoforms of MNKs. The truncated isoform MNK1b, first described in our laboratory, has a higher basal activity and is constitutively active. Aptamers are emerging in recent years as potential therapeutic agents that show significant advantages over drugs of other nature. We have previously obtained and characterized a highly specific aptamer against MNK1b, named apMNK2F, with a dissociation constant in the nanomolar range, which produces significant inhibition of proliferation, migration, and colony formation in breast cancer cells. Furthermore, its sequence analysis predicted two G-quadruplex structures. In this work, we show the optimization process of the aptamer to reduce its size, improving its stability. The obtained aptamer, named apMNKQ2, is able to inhibit proliferation, colony formation, migration, and invasion in breast cancer cells. In murine models of breast cancer, apMNKQ2 has demonstrated its efficacy in reducing tumor volume and the number of metastases. In conclusion, apMNKQ2 could be used as an anti-tumor drug in the future. MT: Oligonucleotides: Therapies and Applications aptamers anti-tumor drug cancer metastasis MNK Therapeutics. Pharmacology R. Ferreras-Martín verfasserin aut R. Carrión-Marchante verfasserin aut J.I. Klett-Mingo verfasserin aut M. García-Hernández verfasserin aut M.I. Pérez-Morgado verfasserin aut S. Sacristán verfasserin aut M. Barragán verfasserin aut M. Seijo-Vila verfasserin aut I. Tundidor verfasserin aut S. Blasco-Benito verfasserin aut E. Pérez-Gómez verfasserin aut I. Gómez-Pinto verfasserin aut C. Sánchez verfasserin aut C. González verfasserin aut V.M. González verfasserin aut M.E. Martín verfasserin aut In Molecular Therapy: Nucleic Acids Elsevier, 2013 30(2022), Seite 553-568 (DE-627)718632702 (DE-600)2662631-7 21622531 nnns volume:30 year:2022 pages:553-568 https://doi.org/10.1016/j.omtn.2022.11.009 kostenfrei https://doaj.org/article/d87a996e039e42de8f35b77109b6aca8 kostenfrei http://www.sciencedirect.com/science/article/pii/S2162253122003018 kostenfrei https://doaj.org/toc/2162-2531 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_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_2336 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 30 2022 553-568
language	English
source	In Molecular Therapy: Nucleic Acids 30(2022), Seite 553-568 volume:30 year:2022 pages:553-568
sourceStr	In Molecular Therapy: Nucleic Acids 30(2022), Seite 553-568 volume:30 year:2022 pages:553-568
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	MT: Oligonucleotides: Therapies and Applications aptamers anti-tumor drug cancer metastasis MNK Therapeutics. Pharmacology
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container_title	Molecular Therapy: Nucleic Acids
authorswithroles_txt_mv	C. Pinto-Díez @@aut@@ R. Ferreras-Martín @@aut@@ R. Carrión-Marchante @@aut@@ J.I. Klett-Mingo @@aut@@ M. García-Hernández @@aut@@ M.I. Pérez-Morgado @@aut@@ S. Sacristán @@aut@@ M. Barragán @@aut@@ M. Seijo-Vila @@aut@@ I. Tundidor @@aut@@ S. Blasco-Benito @@aut@@ E. Pérez-Gómez @@aut@@ I. Gómez-Pinto @@aut@@ C. Sánchez @@aut@@ C. González @@aut@@ V.M. González @@aut@@ M.E. Martín @@aut@@
publishDateDaySort_date	2022-01-01T00:00:00Z
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callnumber-first	R - Medicine
author	C. Pinto-Díez
spellingShingle	C. Pinto-Díez misc RM1-950 misc MT: Oligonucleotides: Therapies and Applications misc aptamers misc anti-tumor drug misc cancer misc metastasis misc MNK misc Therapeutics. Pharmacology An optimized MNK1b aptamer, apMNKQ2, and its potential use as a therapeutic agent in breast cancer
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topic_title	RM1-950 An optimized MNK1b aptamer, apMNKQ2, and its potential use as a therapeutic agent in breast cancer MT: Oligonucleotides: Therapies and Applications aptamers anti-tumor drug cancer metastasis MNK
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title	An optimized MNK1b aptamer, apMNKQ2, and its potential use as a therapeutic agent in breast cancer
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title_full	An optimized MNK1b aptamer, apMNKQ2, and its potential use as a therapeutic agent in breast cancer
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author_browse	C. Pinto-Díez R. Ferreras-Martín R. Carrión-Marchante J.I. Klett-Mingo M. García-Hernández M.I. Pérez-Morgado S. Sacristán M. Barragán M. Seijo-Vila I. Tundidor S. Blasco-Benito E. Pérez-Gómez I. Gómez-Pinto C. Sánchez C. González V.M. González M.E. Martín
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title_sort	optimized mnk1b aptamer, apmnkq2, and its potential use as a therapeutic agent in breast cancer
callnumber	RM1-950
title_auth	An optimized MNK1b aptamer, apMNKQ2, and its potential use as a therapeutic agent in breast cancer
abstract	Breast cancer is the most commonly diagnosed and leading cause of cancer death among women worldwide. Mitogen-activated protein kinase-interacting kinases (MNKs) promote the expression of several oncogenic proteins and are overexpressed in several types of cancer. In human cells, there are four isoforms of MNKs. The truncated isoform MNK1b, first described in our laboratory, has a higher basal activity and is constitutively active. Aptamers are emerging in recent years as potential therapeutic agents that show significant advantages over drugs of other nature. We have previously obtained and characterized a highly specific aptamer against MNK1b, named apMNK2F, with a dissociation constant in the nanomolar range, which produces significant inhibition of proliferation, migration, and colony formation in breast cancer cells. Furthermore, its sequence analysis predicted two G-quadruplex structures. In this work, we show the optimization process of the aptamer to reduce its size, improving its stability. The obtained aptamer, named apMNKQ2, is able to inhibit proliferation, colony formation, migration, and invasion in breast cancer cells. In murine models of breast cancer, apMNKQ2 has demonstrated its efficacy in reducing tumor volume and the number of metastases. In conclusion, apMNKQ2 could be used as an anti-tumor drug in the future.
abstractGer	Breast cancer is the most commonly diagnosed and leading cause of cancer death among women worldwide. Mitogen-activated protein kinase-interacting kinases (MNKs) promote the expression of several oncogenic proteins and are overexpressed in several types of cancer. In human cells, there are four isoforms of MNKs. The truncated isoform MNK1b, first described in our laboratory, has a higher basal activity and is constitutively active. Aptamers are emerging in recent years as potential therapeutic agents that show significant advantages over drugs of other nature. We have previously obtained and characterized a highly specific aptamer against MNK1b, named apMNK2F, with a dissociation constant in the nanomolar range, which produces significant inhibition of proliferation, migration, and colony formation in breast cancer cells. Furthermore, its sequence analysis predicted two G-quadruplex structures. In this work, we show the optimization process of the aptamer to reduce its size, improving its stability. The obtained aptamer, named apMNKQ2, is able to inhibit proliferation, colony formation, migration, and invasion in breast cancer cells. In murine models of breast cancer, apMNKQ2 has demonstrated its efficacy in reducing tumor volume and the number of metastases. In conclusion, apMNKQ2 could be used as an anti-tumor drug in the future.
abstract_unstemmed	Breast cancer is the most commonly diagnosed and leading cause of cancer death among women worldwide. Mitogen-activated protein kinase-interacting kinases (MNKs) promote the expression of several oncogenic proteins and are overexpressed in several types of cancer. In human cells, there are four isoforms of MNKs. The truncated isoform MNK1b, first described in our laboratory, has a higher basal activity and is constitutively active. Aptamers are emerging in recent years as potential therapeutic agents that show significant advantages over drugs of other nature. We have previously obtained and characterized a highly specific aptamer against MNK1b, named apMNK2F, with a dissociation constant in the nanomolar range, which produces significant inhibition of proliferation, migration, and colony formation in breast cancer cells. Furthermore, its sequence analysis predicted two G-quadruplex structures. In this work, we show the optimization process of the aptamer to reduce its size, improving its stability. The obtained aptamer, named apMNKQ2, is able to inhibit proliferation, colony formation, migration, and invasion in breast cancer cells. In murine models of breast cancer, apMNKQ2 has demonstrated its efficacy in reducing tumor volume and the number of metastases. In conclusion, apMNKQ2 could be used as an anti-tumor drug in the future.
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title_short	An optimized MNK1b aptamer, apMNKQ2, and its potential use as a therapeutic agent in breast cancer
url	https://doi.org/10.1016/j.omtn.2022.11.009 https://doaj.org/article/d87a996e039e42de8f35b77109b6aca8 http://www.sciencedirect.com/science/article/pii/S2162253122003018 https://doaj.org/toc/2162-2531
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Pinto-Díez</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="3"><subfield code="a">An optimized MNK1b aptamer, apMNKQ2, and its potential use as a therapeutic agent in breast cancer</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2022</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Breast cancer is the most commonly diagnosed and leading cause of cancer death among women worldwide. Mitogen-activated protein kinase-interacting kinases (MNKs) promote the expression of several oncogenic proteins and are overexpressed in several types of cancer. In human cells, there are four isoforms of MNKs. The truncated isoform MNK1b, first described in our laboratory, has a higher basal activity and is constitutively active. Aptamers are emerging in recent years as potential therapeutic agents that show significant advantages over drugs of other nature. We have previously obtained and characterized a highly specific aptamer against MNK1b, named apMNK2F, with a dissociation constant in the nanomolar range, which produces significant inhibition of proliferation, migration, and colony formation in breast cancer cells. Furthermore, its sequence analysis predicted two G-quadruplex structures. In this work, we show the optimization process of the aptamer to reduce its size, improving its stability. The obtained aptamer, named apMNKQ2, is able to inhibit proliferation, colony formation, migration, and invasion in breast cancer cells. In murine models of breast cancer, apMNKQ2 has demonstrated its efficacy in reducing tumor volume and the number of metastases. 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An optimized MNK1b aptamer, apMNKQ2, and its potential use as a therapeutic agent in breast cancer

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