Recent advances in anti-tumor therapeutic approaches for the universally active transcriptional factor c-MYC

Abstract The universally active transcription factor c-Myc is essential for the regulation of global gene expression and has an impact on many biological functions, including cell division, proliferation, and death. Approximately 70% of human malignancies are caused by dysregulation of c-Myc, contri...
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Autor*in:	Bamrah, Gurpreet Kaur [verfasserIn] Kumari, Neha [verfasserIn] Srivastava, Saurabh [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2024

Schlagwörter:	c-Myc Inhibitors Anti-tumor therapy Proto-oncogene Gene targets

Anmerkung:	© Indian National Science Academy 2024. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.

Übergeordnetes Werk:	Enthalten in: Proceedings of the Indian National Science Academy - Indian National Science Academy, 2022, 90(2024), 3 vom: 23. Feb., Seite 576-593
Übergeordnetes Werk:	volume:90 ; year:2024 ; number:3 ; day:23 ; month:02 ; pages:576-593

Links:	Volltext

DOI / URN:	10.1007/s43538-024-00244-7

Katalog-ID:	SPR057327629

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allfields	10.1007/s43538-024-00244-7 doi (DE-627)SPR057327629 (SPR)s43538-024-00244-7-e DE-627 ger DE-627 rakwb eng Bamrah, Gurpreet Kaur verfasserin aut Recent advances in anti-tumor therapeutic approaches for the universally active transcriptional factor c-MYC 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Indian National Science Academy 2024. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Abstract The universally active transcription factor c-Myc is essential for the regulation of global gene expression and has an impact on many biological functions, including cell division, proliferation, and death. Approximately 70% of human malignancies are caused by dysregulation of c-Myc, contributing to tumor initiation and maintenance. As a result, the therapeutic targeting of c-Myc has attracted considerable interest in the development of cancer drugs. Extensive in vivo studies have demonstrated that inhibition of c-Myc leads to substantial anti-proliferative effects and sustained tumor regression, while remaining reversible in healthy tissues. Despite its pivotal role in cancer progression, the lack of druggable binding pockets and complex protein–protein interaction (PPI) interfaces has traditionally deemed c-Myc as an “undruggable” target. Nevertheless, alternative strategies, such as disrupting the Myc/Max complex, inhibiting Myc transcription and/or translation, destabilizing Myc protein, and exploring synthetic lethality associated with Myc overexpression, have been explored to achieve desirable anti-tumor effects. This review provides a comprehensive overview of recent advancements in targeting oncogenic c-Myc, specifically focusing on its potential as a therapeutic target for cancer treatment. We discuss the underlying mechanisms of c-Myc dysregulation, its impact on cellular pathways, and the challenges associated with developing effective pharmacological inhibitors. Furthermore, we summarize emerging strategies and technologies that have shown promise in tackling the complex network of c-Myc interactions, aiming to develop conceptually innovative and efficient anticancer therapies that can be applied to a wide range of tumors. c-Myc (dpeaa)DE-He213 Inhibitors (dpeaa)DE-He213 Anti-tumor therapy (dpeaa)DE-He213 Proto-oncogene (dpeaa)DE-He213 Gene targets (dpeaa)DE-He213 Kumari, Neha verfasserin aut Srivastava, Saurabh verfasserin (orcid)0000-0002-3032-5557 aut Enthalten in Proceedings of the Indian National Science Academy Indian National Science Academy, 2022 90(2024), 3 vom: 23. Feb., Seite 576-593 (DE-627)78783341X (DE-600)2773381-6 2454-9983 nnns volume:90 year:2024 number:3 day:23 month:02 pages:576-593 https://dx.doi.org/10.1007/s43538-024-00244-7 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 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_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_110 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 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_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 90 2024 3 23 02 576-593
spelling	10.1007/s43538-024-00244-7 doi (DE-627)SPR057327629 (SPR)s43538-024-00244-7-e DE-627 ger DE-627 rakwb eng Bamrah, Gurpreet Kaur verfasserin aut Recent advances in anti-tumor therapeutic approaches for the universally active transcriptional factor c-MYC 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Indian National Science Academy 2024. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Abstract The universally active transcription factor c-Myc is essential for the regulation of global gene expression and has an impact on many biological functions, including cell division, proliferation, and death. Approximately 70% of human malignancies are caused by dysregulation of c-Myc, contributing to tumor initiation and maintenance. As a result, the therapeutic targeting of c-Myc has attracted considerable interest in the development of cancer drugs. Extensive in vivo studies have demonstrated that inhibition of c-Myc leads to substantial anti-proliferative effects and sustained tumor regression, while remaining reversible in healthy tissues. Despite its pivotal role in cancer progression, the lack of druggable binding pockets and complex protein–protein interaction (PPI) interfaces has traditionally deemed c-Myc as an “undruggable” target. Nevertheless, alternative strategies, such as disrupting the Myc/Max complex, inhibiting Myc transcription and/or translation, destabilizing Myc protein, and exploring synthetic lethality associated with Myc overexpression, have been explored to achieve desirable anti-tumor effects. This review provides a comprehensive overview of recent advancements in targeting oncogenic c-Myc, specifically focusing on its potential as a therapeutic target for cancer treatment. We discuss the underlying mechanisms of c-Myc dysregulation, its impact on cellular pathways, and the challenges associated with developing effective pharmacological inhibitors. Furthermore, we summarize emerging strategies and technologies that have shown promise in tackling the complex network of c-Myc interactions, aiming to develop conceptually innovative and efficient anticancer therapies that can be applied to a wide range of tumors. c-Myc (dpeaa)DE-He213 Inhibitors (dpeaa)DE-He213 Anti-tumor therapy (dpeaa)DE-He213 Proto-oncogene (dpeaa)DE-He213 Gene targets (dpeaa)DE-He213 Kumari, Neha verfasserin aut Srivastava, Saurabh verfasserin (orcid)0000-0002-3032-5557 aut Enthalten in Proceedings of the Indian National Science Academy Indian National Science Academy, 2022 90(2024), 3 vom: 23. Feb., Seite 576-593 (DE-627)78783341X (DE-600)2773381-6 2454-9983 nnns volume:90 year:2024 number:3 day:23 month:02 pages:576-593 https://dx.doi.org/10.1007/s43538-024-00244-7 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 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_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_110 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 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_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 90 2024 3 23 02 576-593
allfields_unstemmed	10.1007/s43538-024-00244-7 doi (DE-627)SPR057327629 (SPR)s43538-024-00244-7-e DE-627 ger DE-627 rakwb eng Bamrah, Gurpreet Kaur verfasserin aut Recent advances in anti-tumor therapeutic approaches for the universally active transcriptional factor c-MYC 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Indian National Science Academy 2024. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Abstract The universally active transcription factor c-Myc is essential for the regulation of global gene expression and has an impact on many biological functions, including cell division, proliferation, and death. Approximately 70% of human malignancies are caused by dysregulation of c-Myc, contributing to tumor initiation and maintenance. As a result, the therapeutic targeting of c-Myc has attracted considerable interest in the development of cancer drugs. Extensive in vivo studies have demonstrated that inhibition of c-Myc leads to substantial anti-proliferative effects and sustained tumor regression, while remaining reversible in healthy tissues. Despite its pivotal role in cancer progression, the lack of druggable binding pockets and complex protein–protein interaction (PPI) interfaces has traditionally deemed c-Myc as an “undruggable” target. Nevertheless, alternative strategies, such as disrupting the Myc/Max complex, inhibiting Myc transcription and/or translation, destabilizing Myc protein, and exploring synthetic lethality associated with Myc overexpression, have been explored to achieve desirable anti-tumor effects. This review provides a comprehensive overview of recent advancements in targeting oncogenic c-Myc, specifically focusing on its potential as a therapeutic target for cancer treatment. We discuss the underlying mechanisms of c-Myc dysregulation, its impact on cellular pathways, and the challenges associated with developing effective pharmacological inhibitors. Furthermore, we summarize emerging strategies and technologies that have shown promise in tackling the complex network of c-Myc interactions, aiming to develop conceptually innovative and efficient anticancer therapies that can be applied to a wide range of tumors. c-Myc (dpeaa)DE-He213 Inhibitors (dpeaa)DE-He213 Anti-tumor therapy (dpeaa)DE-He213 Proto-oncogene (dpeaa)DE-He213 Gene targets (dpeaa)DE-He213 Kumari, Neha verfasserin aut Srivastava, Saurabh verfasserin (orcid)0000-0002-3032-5557 aut Enthalten in Proceedings of the Indian National Science Academy Indian National Science Academy, 2022 90(2024), 3 vom: 23. Feb., Seite 576-593 (DE-627)78783341X (DE-600)2773381-6 2454-9983 nnns volume:90 year:2024 number:3 day:23 month:02 pages:576-593 https://dx.doi.org/10.1007/s43538-024-00244-7 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 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_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_110 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 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_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 90 2024 3 23 02 576-593
allfieldsGer	10.1007/s43538-024-00244-7 doi (DE-627)SPR057327629 (SPR)s43538-024-00244-7-e DE-627 ger DE-627 rakwb eng Bamrah, Gurpreet Kaur verfasserin aut Recent advances in anti-tumor therapeutic approaches for the universally active transcriptional factor c-MYC 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Indian National Science Academy 2024. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Abstract The universally active transcription factor c-Myc is essential for the regulation of global gene expression and has an impact on many biological functions, including cell division, proliferation, and death. Approximately 70% of human malignancies are caused by dysregulation of c-Myc, contributing to tumor initiation and maintenance. As a result, the therapeutic targeting of c-Myc has attracted considerable interest in the development of cancer drugs. Extensive in vivo studies have demonstrated that inhibition of c-Myc leads to substantial anti-proliferative effects and sustained tumor regression, while remaining reversible in healthy tissues. Despite its pivotal role in cancer progression, the lack of druggable binding pockets and complex protein–protein interaction (PPI) interfaces has traditionally deemed c-Myc as an “undruggable” target. Nevertheless, alternative strategies, such as disrupting the Myc/Max complex, inhibiting Myc transcription and/or translation, destabilizing Myc protein, and exploring synthetic lethality associated with Myc overexpression, have been explored to achieve desirable anti-tumor effects. This review provides a comprehensive overview of recent advancements in targeting oncogenic c-Myc, specifically focusing on its potential as a therapeutic target for cancer treatment. We discuss the underlying mechanisms of c-Myc dysregulation, its impact on cellular pathways, and the challenges associated with developing effective pharmacological inhibitors. Furthermore, we summarize emerging strategies and technologies that have shown promise in tackling the complex network of c-Myc interactions, aiming to develop conceptually innovative and efficient anticancer therapies that can be applied to a wide range of tumors. c-Myc (dpeaa)DE-He213 Inhibitors (dpeaa)DE-He213 Anti-tumor therapy (dpeaa)DE-He213 Proto-oncogene (dpeaa)DE-He213 Gene targets (dpeaa)DE-He213 Kumari, Neha verfasserin aut Srivastava, Saurabh verfasserin (orcid)0000-0002-3032-5557 aut Enthalten in Proceedings of the Indian National Science Academy Indian National Science Academy, 2022 90(2024), 3 vom: 23. Feb., Seite 576-593 (DE-627)78783341X (DE-600)2773381-6 2454-9983 nnns volume:90 year:2024 number:3 day:23 month:02 pages:576-593 https://dx.doi.org/10.1007/s43538-024-00244-7 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 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_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_110 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 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_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 90 2024 3 23 02 576-593
allfieldsSound	10.1007/s43538-024-00244-7 doi (DE-627)SPR057327629 (SPR)s43538-024-00244-7-e DE-627 ger DE-627 rakwb eng Bamrah, Gurpreet Kaur verfasserin aut Recent advances in anti-tumor therapeutic approaches for the universally active transcriptional factor c-MYC 2024 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Indian National Science Academy 2024. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Abstract The universally active transcription factor c-Myc is essential for the regulation of global gene expression and has an impact on many biological functions, including cell division, proliferation, and death. Approximately 70% of human malignancies are caused by dysregulation of c-Myc, contributing to tumor initiation and maintenance. As a result, the therapeutic targeting of c-Myc has attracted considerable interest in the development of cancer drugs. Extensive in vivo studies have demonstrated that inhibition of c-Myc leads to substantial anti-proliferative effects and sustained tumor regression, while remaining reversible in healthy tissues. Despite its pivotal role in cancer progression, the lack of druggable binding pockets and complex protein–protein interaction (PPI) interfaces has traditionally deemed c-Myc as an “undruggable” target. Nevertheless, alternative strategies, such as disrupting the Myc/Max complex, inhibiting Myc transcription and/or translation, destabilizing Myc protein, and exploring synthetic lethality associated with Myc overexpression, have been explored to achieve desirable anti-tumor effects. This review provides a comprehensive overview of recent advancements in targeting oncogenic c-Myc, specifically focusing on its potential as a therapeutic target for cancer treatment. We discuss the underlying mechanisms of c-Myc dysregulation, its impact on cellular pathways, and the challenges associated with developing effective pharmacological inhibitors. Furthermore, we summarize emerging strategies and technologies that have shown promise in tackling the complex network of c-Myc interactions, aiming to develop conceptually innovative and efficient anticancer therapies that can be applied to a wide range of tumors. c-Myc (dpeaa)DE-He213 Inhibitors (dpeaa)DE-He213 Anti-tumor therapy (dpeaa)DE-He213 Proto-oncogene (dpeaa)DE-He213 Gene targets (dpeaa)DE-He213 Kumari, Neha verfasserin aut Srivastava, Saurabh verfasserin (orcid)0000-0002-3032-5557 aut Enthalten in Proceedings of the Indian National Science Academy Indian National Science Academy, 2022 90(2024), 3 vom: 23. Feb., Seite 576-593 (DE-627)78783341X (DE-600)2773381-6 2454-9983 nnns volume:90 year:2024 number:3 day:23 month:02 pages:576-593 https://dx.doi.org/10.1007/s43538-024-00244-7 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 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_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_110 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 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_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 90 2024 3 23 02 576-593
language	English
source	Enthalten in Proceedings of the Indian National Science Academy 90(2024), 3 vom: 23. Feb., Seite 576-593 volume:90 year:2024 number:3 day:23 month:02 pages:576-593
sourceStr	Enthalten in Proceedings of the Indian National Science Academy 90(2024), 3 vom: 23. Feb., Seite 576-593 volume:90 year:2024 number:3 day:23 month:02 pages:576-593
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	c-Myc Inhibitors Anti-tumor therapy Proto-oncogene Gene targets
isfreeaccess_bool	false
container_title	Proceedings of the Indian National Science Academy
authorswithroles_txt_mv	Bamrah, Gurpreet Kaur @@aut@@ Kumari, Neha @@aut@@ Srivastava, Saurabh @@aut@@
publishDateDaySort_date	2024-02-23T00:00:00Z
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author	Bamrah, Gurpreet Kaur
spellingShingle	Bamrah, Gurpreet Kaur misc c-Myc misc Inhibitors misc Anti-tumor therapy misc Proto-oncogene misc Gene targets Recent advances in anti-tumor therapeutic approaches for the universally active transcriptional factor c-MYC
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topic_title	Recent advances in anti-tumor therapeutic approaches for the universally active transcriptional factor c-MYC c-Myc (dpeaa)DE-He213 Inhibitors (dpeaa)DE-He213 Anti-tumor therapy (dpeaa)DE-He213 Proto-oncogene (dpeaa)DE-He213 Gene targets (dpeaa)DE-He213
topic	misc c-Myc misc Inhibitors misc Anti-tumor therapy misc Proto-oncogene misc Gene targets
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title	Recent advances in anti-tumor therapeutic approaches for the universally active transcriptional factor c-MYC
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title_full	Recent advances in anti-tumor therapeutic approaches for the universally active transcriptional factor c-MYC
author_sort	Bamrah, Gurpreet Kaur
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title_sort	recent advances in anti-tumor therapeutic approaches for the universally active transcriptional factor c-myc
title_auth	Recent advances in anti-tumor therapeutic approaches for the universally active transcriptional factor c-MYC
abstract	Abstract The universally active transcription factor c-Myc is essential for the regulation of global gene expression and has an impact on many biological functions, including cell division, proliferation, and death. Approximately 70% of human malignancies are caused by dysregulation of c-Myc, contributing to tumor initiation and maintenance. As a result, the therapeutic targeting of c-Myc has attracted considerable interest in the development of cancer drugs. Extensive in vivo studies have demonstrated that inhibition of c-Myc leads to substantial anti-proliferative effects and sustained tumor regression, while remaining reversible in healthy tissues. Despite its pivotal role in cancer progression, the lack of druggable binding pockets and complex protein–protein interaction (PPI) interfaces has traditionally deemed c-Myc as an “undruggable” target. Nevertheless, alternative strategies, such as disrupting the Myc/Max complex, inhibiting Myc transcription and/or translation, destabilizing Myc protein, and exploring synthetic lethality associated with Myc overexpression, have been explored to achieve desirable anti-tumor effects. This review provides a comprehensive overview of recent advancements in targeting oncogenic c-Myc, specifically focusing on its potential as a therapeutic target for cancer treatment. We discuss the underlying mechanisms of c-Myc dysregulation, its impact on cellular pathways, and the challenges associated with developing effective pharmacological inhibitors. Furthermore, we summarize emerging strategies and technologies that have shown promise in tackling the complex network of c-Myc interactions, aiming to develop conceptually innovative and efficient anticancer therapies that can be applied to a wide range of tumors. © Indian National Science Academy 2024. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.
abstractGer	Abstract The universally active transcription factor c-Myc is essential for the regulation of global gene expression and has an impact on many biological functions, including cell division, proliferation, and death. Approximately 70% of human malignancies are caused by dysregulation of c-Myc, contributing to tumor initiation and maintenance. As a result, the therapeutic targeting of c-Myc has attracted considerable interest in the development of cancer drugs. Extensive in vivo studies have demonstrated that inhibition of c-Myc leads to substantial anti-proliferative effects and sustained tumor regression, while remaining reversible in healthy tissues. Despite its pivotal role in cancer progression, the lack of druggable binding pockets and complex protein–protein interaction (PPI) interfaces has traditionally deemed c-Myc as an “undruggable” target. Nevertheless, alternative strategies, such as disrupting the Myc/Max complex, inhibiting Myc transcription and/or translation, destabilizing Myc protein, and exploring synthetic lethality associated with Myc overexpression, have been explored to achieve desirable anti-tumor effects. This review provides a comprehensive overview of recent advancements in targeting oncogenic c-Myc, specifically focusing on its potential as a therapeutic target for cancer treatment. We discuss the underlying mechanisms of c-Myc dysregulation, its impact on cellular pathways, and the challenges associated with developing effective pharmacological inhibitors. Furthermore, we summarize emerging strategies and technologies that have shown promise in tackling the complex network of c-Myc interactions, aiming to develop conceptually innovative and efficient anticancer therapies that can be applied to a wide range of tumors. © Indian National Science Academy 2024. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.
abstract_unstemmed	Abstract The universally active transcription factor c-Myc is essential for the regulation of global gene expression and has an impact on many biological functions, including cell division, proliferation, and death. Approximately 70% of human malignancies are caused by dysregulation of c-Myc, contributing to tumor initiation and maintenance. As a result, the therapeutic targeting of c-Myc has attracted considerable interest in the development of cancer drugs. Extensive in vivo studies have demonstrated that inhibition of c-Myc leads to substantial anti-proliferative effects and sustained tumor regression, while remaining reversible in healthy tissues. Despite its pivotal role in cancer progression, the lack of druggable binding pockets and complex protein–protein interaction (PPI) interfaces has traditionally deemed c-Myc as an “undruggable” target. Nevertheless, alternative strategies, such as disrupting the Myc/Max complex, inhibiting Myc transcription and/or translation, destabilizing Myc protein, and exploring synthetic lethality associated with Myc overexpression, have been explored to achieve desirable anti-tumor effects. This review provides a comprehensive overview of recent advancements in targeting oncogenic c-Myc, specifically focusing on its potential as a therapeutic target for cancer treatment. We discuss the underlying mechanisms of c-Myc dysregulation, its impact on cellular pathways, and the challenges associated with developing effective pharmacological inhibitors. Furthermore, we summarize emerging strategies and technologies that have shown promise in tackling the complex network of c-Myc interactions, aiming to develop conceptually innovative and efficient anticancer therapies that can be applied to a wide range of tumors. © Indian National Science Academy 2024. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.
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title_short	Recent advances in anti-tumor therapeutic approaches for the universally active transcriptional factor c-MYC
url	https://dx.doi.org/10.1007/s43538-024-00244-7
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author2	Kumari, Neha Srivastava, Saurabh
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doi_str	10.1007/s43538-024-00244-7
up_date	2024-09-14T04:49:08.808Z
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Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract The universally active transcription factor c-Myc is essential for the regulation of global gene expression and has an impact on many biological functions, including cell division, proliferation, and death. Approximately 70% of human malignancies are caused by dysregulation of c-Myc, contributing to tumor initiation and maintenance. As a result, the therapeutic targeting of c-Myc has attracted considerable interest in the development of cancer drugs. Extensive in vivo studies have demonstrated that inhibition of c-Myc leads to substantial anti-proliferative effects and sustained tumor regression, while remaining reversible in healthy tissues. Despite its pivotal role in cancer progression, the lack of druggable binding pockets and complex protein–protein interaction (PPI) interfaces has traditionally deemed c-Myc as an “undruggable” target. Nevertheless, alternative strategies, such as disrupting the Myc/Max complex, inhibiting Myc transcription and/or translation, destabilizing Myc protein, and exploring synthetic lethality associated with Myc overexpression, have been explored to achieve desirable anti-tumor effects. This review provides a comprehensive overview of recent advancements in targeting oncogenic c-Myc, specifically focusing on its potential as a therapeutic target for cancer treatment. 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