Aptamer-miR-34c Conjugate Affects Cell Proliferation of Non-Small-Cell Lung Cancer Cells

MicroRNAs (miRNAs) are key regulators of different human processes that represent a new promising class of cancer therapeutics or therapeutic targets. Indeed, in several tumor types, including non-small-cell lung carcinoma (NSCLC), the deregulated expression of specific miRNAs has been implicated in...
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Autor*in:	Valentina Russo [verfasserIn] Alessia Paciocco [verfasserIn] Alessandra Affinito [verfasserIn] Giuseppina Roscigno [verfasserIn] Danilo Fiore [verfasserIn] Francesco Palma [verfasserIn] Marco Galasso [verfasserIn] Stefano Volinia [verfasserIn] Alfonso Fiorelli [verfasserIn] Carla Lucia Esposito [verfasserIn] Silvia Nuzzo [verfasserIn] Giorgio Inghirami [verfasserIn] Vittorio de Franciscis [verfasserIn] Gerolama Condorelli [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2018

Übergeordnetes Werk:	In: Molecular Therapy: Nucleic Acids - Elsevier, 2013, 13(2018), Seite 334-346
Übergeordnetes Werk:	volume:13 ; year:2018 ; pages:334-346

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1016/j.omtn.2018.09.016

Katalog-ID:	DOAJ034592644

Internformat


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520			\|a MicroRNAs (miRNAs) are key regulators of different human processes that represent a new promising class of cancer therapeutics or therapeutic targets. Indeed, in several tumor types, including non-small-cell lung carcinoma (NSCLC), the deregulated expression of specific miRNAs has been implicated in cell malignancy. As expression levels of the oncosuppressor miR-34c-3p are decreased in NSCLC compared to normal lung, we show that reintroduction of miR-34c-3p reduces NSCLC cell survival in vitro. Further, in order to deliver the miR-34c-based therapeutic selectively to tumor cells, we took advantage of a reported nucleic acid aptamer (GL21.T) that binds and inhibits the AXL transmembrane receptor and is rapidly internalized in the target cells. By applying methods successfully used in our laboratory, we conjugated miR-34c to the GL21.T aptamer as targeting moiety for the selective delivery to AXL-expressing NSCLC cells. We demonstrate that miR-34c-3p and the GL21.T/miR-34c chimera affect NSCLC cell proliferation and are able to overcome acquired RTK-inhibitor resistance by targeting AXL receptor. Thus, the GL21.T/miR-34c chimera exerts dual inhibition of AXL at functional and transcriptional levels and represents a novel therapeutic tool for the treatment of NSCLC. Keywords: miRNA, aptamer, NSCLC, lung cancer, therapeutics
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allfields	10.1016/j.omtn.2018.09.016 doi (DE-627)DOAJ034592644 (DE-599)DOAJc076190e86e845b698c2077731266200 DE-627 ger DE-627 rakwb eng RM1-950 Valentina Russo verfasserin aut Aptamer-miR-34c Conjugate Affects Cell Proliferation of Non-Small-Cell Lung Cancer Cells 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier MicroRNAs (miRNAs) are key regulators of different human processes that represent a new promising class of cancer therapeutics or therapeutic targets. Indeed, in several tumor types, including non-small-cell lung carcinoma (NSCLC), the deregulated expression of specific miRNAs has been implicated in cell malignancy. As expression levels of the oncosuppressor miR-34c-3p are decreased in NSCLC compared to normal lung, we show that reintroduction of miR-34c-3p reduces NSCLC cell survival in vitro. Further, in order to deliver the miR-34c-based therapeutic selectively to tumor cells, we took advantage of a reported nucleic acid aptamer (GL21.T) that binds and inhibits the AXL transmembrane receptor and is rapidly internalized in the target cells. By applying methods successfully used in our laboratory, we conjugated miR-34c to the GL21.T aptamer as targeting moiety for the selective delivery to AXL-expressing NSCLC cells. We demonstrate that miR-34c-3p and the GL21.T/miR-34c chimera affect NSCLC cell proliferation and are able to overcome acquired RTK-inhibitor resistance by targeting AXL receptor. Thus, the GL21.T/miR-34c chimera exerts dual inhibition of AXL at functional and transcriptional levels and represents a novel therapeutic tool for the treatment of NSCLC. Keywords: miRNA, aptamer, NSCLC, lung cancer, therapeutics Therapeutics. Pharmacology Alessia Paciocco verfasserin aut Alessandra Affinito verfasserin aut Giuseppina Roscigno verfasserin aut Danilo Fiore verfasserin aut Francesco Palma verfasserin aut Marco Galasso verfasserin aut Stefano Volinia verfasserin aut Alfonso Fiorelli verfasserin aut Carla Lucia Esposito verfasserin aut Silvia Nuzzo verfasserin aut Giorgio Inghirami verfasserin aut Vittorio de Franciscis verfasserin aut Gerolama Condorelli verfasserin aut In Molecular Therapy: Nucleic Acids Elsevier, 2013 13(2018), Seite 334-346 (DE-627)718632702 (DE-600)2662631-7 21622531 nnns volume:13 year:2018 pages:334-346 https://doi.org/10.1016/j.omtn.2018.09.016 kostenfrei https://doaj.org/article/c076190e86e845b698c2077731266200 kostenfrei http://www.sciencedirect.com/science/article/pii/S2162253118302609 kostenfrei https://doaj.org/toc/2162-2531 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA 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 13 2018 334-346
spelling	10.1016/j.omtn.2018.09.016 doi (DE-627)DOAJ034592644 (DE-599)DOAJc076190e86e845b698c2077731266200 DE-627 ger DE-627 rakwb eng RM1-950 Valentina Russo verfasserin aut Aptamer-miR-34c Conjugate Affects Cell Proliferation of Non-Small-Cell Lung Cancer Cells 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier MicroRNAs (miRNAs) are key regulators of different human processes that represent a new promising class of cancer therapeutics or therapeutic targets. Indeed, in several tumor types, including non-small-cell lung carcinoma (NSCLC), the deregulated expression of specific miRNAs has been implicated in cell malignancy. As expression levels of the oncosuppressor miR-34c-3p are decreased in NSCLC compared to normal lung, we show that reintroduction of miR-34c-3p reduces NSCLC cell survival in vitro. Further, in order to deliver the miR-34c-based therapeutic selectively to tumor cells, we took advantage of a reported nucleic acid aptamer (GL21.T) that binds and inhibits the AXL transmembrane receptor and is rapidly internalized in the target cells. By applying methods successfully used in our laboratory, we conjugated miR-34c to the GL21.T aptamer as targeting moiety for the selective delivery to AXL-expressing NSCLC cells. We demonstrate that miR-34c-3p and the GL21.T/miR-34c chimera affect NSCLC cell proliferation and are able to overcome acquired RTK-inhibitor resistance by targeting AXL receptor. Thus, the GL21.T/miR-34c chimera exerts dual inhibition of AXL at functional and transcriptional levels and represents a novel therapeutic tool for the treatment of NSCLC. Keywords: miRNA, aptamer, NSCLC, lung cancer, therapeutics Therapeutics. Pharmacology Alessia Paciocco verfasserin aut Alessandra Affinito verfasserin aut Giuseppina Roscigno verfasserin aut Danilo Fiore verfasserin aut Francesco Palma verfasserin aut Marco Galasso verfasserin aut Stefano Volinia verfasserin aut Alfonso Fiorelli verfasserin aut Carla Lucia Esposito verfasserin aut Silvia Nuzzo verfasserin aut Giorgio Inghirami verfasserin aut Vittorio de Franciscis verfasserin aut Gerolama Condorelli verfasserin aut In Molecular Therapy: Nucleic Acids Elsevier, 2013 13(2018), Seite 334-346 (DE-627)718632702 (DE-600)2662631-7 21622531 nnns volume:13 year:2018 pages:334-346 https://doi.org/10.1016/j.omtn.2018.09.016 kostenfrei https://doaj.org/article/c076190e86e845b698c2077731266200 kostenfrei http://www.sciencedirect.com/science/article/pii/S2162253118302609 kostenfrei https://doaj.org/toc/2162-2531 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA 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 13 2018 334-346
allfields_unstemmed	10.1016/j.omtn.2018.09.016 doi (DE-627)DOAJ034592644 (DE-599)DOAJc076190e86e845b698c2077731266200 DE-627 ger DE-627 rakwb eng RM1-950 Valentina Russo verfasserin aut Aptamer-miR-34c Conjugate Affects Cell Proliferation of Non-Small-Cell Lung Cancer Cells 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier MicroRNAs (miRNAs) are key regulators of different human processes that represent a new promising class of cancer therapeutics or therapeutic targets. Indeed, in several tumor types, including non-small-cell lung carcinoma (NSCLC), the deregulated expression of specific miRNAs has been implicated in cell malignancy. As expression levels of the oncosuppressor miR-34c-3p are decreased in NSCLC compared to normal lung, we show that reintroduction of miR-34c-3p reduces NSCLC cell survival in vitro. Further, in order to deliver the miR-34c-based therapeutic selectively to tumor cells, we took advantage of a reported nucleic acid aptamer (GL21.T) that binds and inhibits the AXL transmembrane receptor and is rapidly internalized in the target cells. By applying methods successfully used in our laboratory, we conjugated miR-34c to the GL21.T aptamer as targeting moiety for the selective delivery to AXL-expressing NSCLC cells. We demonstrate that miR-34c-3p and the GL21.T/miR-34c chimera affect NSCLC cell proliferation and are able to overcome acquired RTK-inhibitor resistance by targeting AXL receptor. Thus, the GL21.T/miR-34c chimera exerts dual inhibition of AXL at functional and transcriptional levels and represents a novel therapeutic tool for the treatment of NSCLC. Keywords: miRNA, aptamer, NSCLC, lung cancer, therapeutics Therapeutics. Pharmacology Alessia Paciocco verfasserin aut Alessandra Affinito verfasserin aut Giuseppina Roscigno verfasserin aut Danilo Fiore verfasserin aut Francesco Palma verfasserin aut Marco Galasso verfasserin aut Stefano Volinia verfasserin aut Alfonso Fiorelli verfasserin aut Carla Lucia Esposito verfasserin aut Silvia Nuzzo verfasserin aut Giorgio Inghirami verfasserin aut Vittorio de Franciscis verfasserin aut Gerolama Condorelli verfasserin aut In Molecular Therapy: Nucleic Acids Elsevier, 2013 13(2018), Seite 334-346 (DE-627)718632702 (DE-600)2662631-7 21622531 nnns volume:13 year:2018 pages:334-346 https://doi.org/10.1016/j.omtn.2018.09.016 kostenfrei https://doaj.org/article/c076190e86e845b698c2077731266200 kostenfrei http://www.sciencedirect.com/science/article/pii/S2162253118302609 kostenfrei https://doaj.org/toc/2162-2531 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA 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 13 2018 334-346
allfieldsGer	10.1016/j.omtn.2018.09.016 doi (DE-627)DOAJ034592644 (DE-599)DOAJc076190e86e845b698c2077731266200 DE-627 ger DE-627 rakwb eng RM1-950 Valentina Russo verfasserin aut Aptamer-miR-34c Conjugate Affects Cell Proliferation of Non-Small-Cell Lung Cancer Cells 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier MicroRNAs (miRNAs) are key regulators of different human processes that represent a new promising class of cancer therapeutics or therapeutic targets. Indeed, in several tumor types, including non-small-cell lung carcinoma (NSCLC), the deregulated expression of specific miRNAs has been implicated in cell malignancy. As expression levels of the oncosuppressor miR-34c-3p are decreased in NSCLC compared to normal lung, we show that reintroduction of miR-34c-3p reduces NSCLC cell survival in vitro. Further, in order to deliver the miR-34c-based therapeutic selectively to tumor cells, we took advantage of a reported nucleic acid aptamer (GL21.T) that binds and inhibits the AXL transmembrane receptor and is rapidly internalized in the target cells. By applying methods successfully used in our laboratory, we conjugated miR-34c to the GL21.T aptamer as targeting moiety for the selective delivery to AXL-expressing NSCLC cells. We demonstrate that miR-34c-3p and the GL21.T/miR-34c chimera affect NSCLC cell proliferation and are able to overcome acquired RTK-inhibitor resistance by targeting AXL receptor. Thus, the GL21.T/miR-34c chimera exerts dual inhibition of AXL at functional and transcriptional levels and represents a novel therapeutic tool for the treatment of NSCLC. Keywords: miRNA, aptamer, NSCLC, lung cancer, therapeutics Therapeutics. Pharmacology Alessia Paciocco verfasserin aut Alessandra Affinito verfasserin aut Giuseppina Roscigno verfasserin aut Danilo Fiore verfasserin aut Francesco Palma verfasserin aut Marco Galasso verfasserin aut Stefano Volinia verfasserin aut Alfonso Fiorelli verfasserin aut Carla Lucia Esposito verfasserin aut Silvia Nuzzo verfasserin aut Giorgio Inghirami verfasserin aut Vittorio de Franciscis verfasserin aut Gerolama Condorelli verfasserin aut In Molecular Therapy: Nucleic Acids Elsevier, 2013 13(2018), Seite 334-346 (DE-627)718632702 (DE-600)2662631-7 21622531 nnns volume:13 year:2018 pages:334-346 https://doi.org/10.1016/j.omtn.2018.09.016 kostenfrei https://doaj.org/article/c076190e86e845b698c2077731266200 kostenfrei http://www.sciencedirect.com/science/article/pii/S2162253118302609 kostenfrei https://doaj.org/toc/2162-2531 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA 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 13 2018 334-346
allfieldsSound	10.1016/j.omtn.2018.09.016 doi (DE-627)DOAJ034592644 (DE-599)DOAJc076190e86e845b698c2077731266200 DE-627 ger DE-627 rakwb eng RM1-950 Valentina Russo verfasserin aut Aptamer-miR-34c Conjugate Affects Cell Proliferation of Non-Small-Cell Lung Cancer Cells 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier MicroRNAs (miRNAs) are key regulators of different human processes that represent a new promising class of cancer therapeutics or therapeutic targets. Indeed, in several tumor types, including non-small-cell lung carcinoma (NSCLC), the deregulated expression of specific miRNAs has been implicated in cell malignancy. As expression levels of the oncosuppressor miR-34c-3p are decreased in NSCLC compared to normal lung, we show that reintroduction of miR-34c-3p reduces NSCLC cell survival in vitro. Further, in order to deliver the miR-34c-based therapeutic selectively to tumor cells, we took advantage of a reported nucleic acid aptamer (GL21.T) that binds and inhibits the AXL transmembrane receptor and is rapidly internalized in the target cells. By applying methods successfully used in our laboratory, we conjugated miR-34c to the GL21.T aptamer as targeting moiety for the selective delivery to AXL-expressing NSCLC cells. We demonstrate that miR-34c-3p and the GL21.T/miR-34c chimera affect NSCLC cell proliferation and are able to overcome acquired RTK-inhibitor resistance by targeting AXL receptor. Thus, the GL21.T/miR-34c chimera exerts dual inhibition of AXL at functional and transcriptional levels and represents a novel therapeutic tool for the treatment of NSCLC. Keywords: miRNA, aptamer, NSCLC, lung cancer, therapeutics Therapeutics. Pharmacology Alessia Paciocco verfasserin aut Alessandra Affinito verfasserin aut Giuseppina Roscigno verfasserin aut Danilo Fiore verfasserin aut Francesco Palma verfasserin aut Marco Galasso verfasserin aut Stefano Volinia verfasserin aut Alfonso Fiorelli verfasserin aut Carla Lucia Esposito verfasserin aut Silvia Nuzzo verfasserin aut Giorgio Inghirami verfasserin aut Vittorio de Franciscis verfasserin aut Gerolama Condorelli verfasserin aut In Molecular Therapy: Nucleic Acids Elsevier, 2013 13(2018), Seite 334-346 (DE-627)718632702 (DE-600)2662631-7 21622531 nnns volume:13 year:2018 pages:334-346 https://doi.org/10.1016/j.omtn.2018.09.016 kostenfrei https://doaj.org/article/c076190e86e845b698c2077731266200 kostenfrei http://www.sciencedirect.com/science/article/pii/S2162253118302609 kostenfrei https://doaj.org/toc/2162-2531 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA 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 13 2018 334-346
language	English
source	In Molecular Therapy: Nucleic Acids 13(2018), Seite 334-346 volume:13 year:2018 pages:334-346
sourceStr	In Molecular Therapy: Nucleic Acids 13(2018), Seite 334-346 volume:13 year:2018 pages:334-346
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Therapeutics. Pharmacology
isfreeaccess_bool	true
container_title	Molecular Therapy: Nucleic Acids
authorswithroles_txt_mv	Valentina Russo @@aut@@ Alessia Paciocco @@aut@@ Alessandra Affinito @@aut@@ Giuseppina Roscigno @@aut@@ Danilo Fiore @@aut@@ Francesco Palma @@aut@@ Marco Galasso @@aut@@ Stefano Volinia @@aut@@ Alfonso Fiorelli @@aut@@ Carla Lucia Esposito @@aut@@ Silvia Nuzzo @@aut@@ Giorgio Inghirami @@aut@@ Vittorio de Franciscis @@aut@@ Gerolama Condorelli @@aut@@
publishDateDaySort_date	2018-01-01T00:00:00Z
hierarchy_top_id	718632702
id	DOAJ034592644
language_de	englisch
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callnumber-first	R - Medicine
author	Valentina Russo
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topic_title	RM1-950 Aptamer-miR-34c Conjugate Affects Cell Proliferation of Non-Small-Cell Lung Cancer Cells
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title	Aptamer-miR-34c Conjugate Affects Cell Proliferation of Non-Small-Cell Lung Cancer Cells
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title_full	Aptamer-miR-34c Conjugate Affects Cell Proliferation of Non-Small-Cell Lung Cancer Cells
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author_browse	Valentina Russo Alessia Paciocco Alessandra Affinito Giuseppina Roscigno Danilo Fiore Francesco Palma Marco Galasso Stefano Volinia Alfonso Fiorelli Carla Lucia Esposito Silvia Nuzzo Giorgio Inghirami Vittorio de Franciscis Gerolama Condorelli
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title_sort	aptamer-mir-34c conjugate affects cell proliferation of non-small-cell lung cancer cells
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title_auth	Aptamer-miR-34c Conjugate Affects Cell Proliferation of Non-Small-Cell Lung Cancer Cells
abstract	MicroRNAs (miRNAs) are key regulators of different human processes that represent a new promising class of cancer therapeutics or therapeutic targets. Indeed, in several tumor types, including non-small-cell lung carcinoma (NSCLC), the deregulated expression of specific miRNAs has been implicated in cell malignancy. As expression levels of the oncosuppressor miR-34c-3p are decreased in NSCLC compared to normal lung, we show that reintroduction of miR-34c-3p reduces NSCLC cell survival in vitro. Further, in order to deliver the miR-34c-based therapeutic selectively to tumor cells, we took advantage of a reported nucleic acid aptamer (GL21.T) that binds and inhibits the AXL transmembrane receptor and is rapidly internalized in the target cells. By applying methods successfully used in our laboratory, we conjugated miR-34c to the GL21.T aptamer as targeting moiety for the selective delivery to AXL-expressing NSCLC cells. We demonstrate that miR-34c-3p and the GL21.T/miR-34c chimera affect NSCLC cell proliferation and are able to overcome acquired RTK-inhibitor resistance by targeting AXL receptor. Thus, the GL21.T/miR-34c chimera exerts dual inhibition of AXL at functional and transcriptional levels and represents a novel therapeutic tool for the treatment of NSCLC. Keywords: miRNA, aptamer, NSCLC, lung cancer, therapeutics
abstractGer	MicroRNAs (miRNAs) are key regulators of different human processes that represent a new promising class of cancer therapeutics or therapeutic targets. Indeed, in several tumor types, including non-small-cell lung carcinoma (NSCLC), the deregulated expression of specific miRNAs has been implicated in cell malignancy. As expression levels of the oncosuppressor miR-34c-3p are decreased in NSCLC compared to normal lung, we show that reintroduction of miR-34c-3p reduces NSCLC cell survival in vitro. Further, in order to deliver the miR-34c-based therapeutic selectively to tumor cells, we took advantage of a reported nucleic acid aptamer (GL21.T) that binds and inhibits the AXL transmembrane receptor and is rapidly internalized in the target cells. By applying methods successfully used in our laboratory, we conjugated miR-34c to the GL21.T aptamer as targeting moiety for the selective delivery to AXL-expressing NSCLC cells. We demonstrate that miR-34c-3p and the GL21.T/miR-34c chimera affect NSCLC cell proliferation and are able to overcome acquired RTK-inhibitor resistance by targeting AXL receptor. Thus, the GL21.T/miR-34c chimera exerts dual inhibition of AXL at functional and transcriptional levels and represents a novel therapeutic tool for the treatment of NSCLC. Keywords: miRNA, aptamer, NSCLC, lung cancer, therapeutics
abstract_unstemmed	MicroRNAs (miRNAs) are key regulators of different human processes that represent a new promising class of cancer therapeutics or therapeutic targets. Indeed, in several tumor types, including non-small-cell lung carcinoma (NSCLC), the deregulated expression of specific miRNAs has been implicated in cell malignancy. As expression levels of the oncosuppressor miR-34c-3p are decreased in NSCLC compared to normal lung, we show that reintroduction of miR-34c-3p reduces NSCLC cell survival in vitro. Further, in order to deliver the miR-34c-based therapeutic selectively to tumor cells, we took advantage of a reported nucleic acid aptamer (GL21.T) that binds and inhibits the AXL transmembrane receptor and is rapidly internalized in the target cells. By applying methods successfully used in our laboratory, we conjugated miR-34c to the GL21.T aptamer as targeting moiety for the selective delivery to AXL-expressing NSCLC cells. We demonstrate that miR-34c-3p and the GL21.T/miR-34c chimera affect NSCLC cell proliferation and are able to overcome acquired RTK-inhibitor resistance by targeting AXL receptor. Thus, the GL21.T/miR-34c chimera exerts dual inhibition of AXL at functional and transcriptional levels and represents a novel therapeutic tool for the treatment of NSCLC. Keywords: miRNA, aptamer, NSCLC, lung cancer, therapeutics
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title_short	Aptamer-miR-34c Conjugate Affects Cell Proliferation of Non-Small-Cell Lung Cancer Cells
url	https://doi.org/10.1016/j.omtn.2018.09.016 https://doaj.org/article/c076190e86e845b698c2077731266200 http://www.sciencedirect.com/science/article/pii/S2162253118302609 https://doaj.org/toc/2162-2531
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author2Str	Alessia Paciocco Alessandra Affinito Giuseppina Roscigno Danilo Fiore Francesco Palma Marco Galasso Stefano Volinia Alfonso Fiorelli Carla Lucia Esposito Silvia Nuzzo Giorgio Inghirami Vittorio de Franciscis Gerolama Condorelli
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up_date	2024-07-03T23:51:23.238Z
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Indeed, in several tumor types, including non-small-cell lung carcinoma (NSCLC), the deregulated expression of specific miRNAs has been implicated in cell malignancy. As expression levels of the oncosuppressor miR-34c-3p are decreased in NSCLC compared to normal lung, we show that reintroduction of miR-34c-3p reduces NSCLC cell survival in vitro. Further, in order to deliver the miR-34c-based therapeutic selectively to tumor cells, we took advantage of a reported nucleic acid aptamer (GL21.T) that binds and inhibits the AXL transmembrane receptor and is rapidly internalized in the target cells. By applying methods successfully used in our laboratory, we conjugated miR-34c to the GL21.T aptamer as targeting moiety for the selective delivery to AXL-expressing NSCLC cells. We demonstrate that miR-34c-3p and the GL21.T/miR-34c chimera affect NSCLC cell proliferation and are able to overcome acquired RTK-inhibitor resistance by targeting AXL receptor. 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Aptamer-miR-34c Conjugate Affects Cell Proliferation of Non-Small-Cell Lung Cancer Cells

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