Metabostemness in cancer: Linking metaboloepigenetics and mitophagy in remodeling cancer stem cells
Cancer stem cells (CSCs) are rare populations of malignant cells with stem cell-like features of self-renewal, uninterrupted differentiation, tumorigenicity, and resistance to conventional therapeutic agents, and these cells have a decisive role in treatment failure and tumor relapse. The self-renew...
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| Autor*in: |
Naik, Prajna Paramita [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2021 |
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| Schlagwörter: |
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| Anmerkung: |
© The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021 |
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| Übergeordnetes Werk: |
Enthalten in: Stem cell reviews - New York, NY : Springer, 2005, 18(2021), 1 vom: 05. Aug., Seite 198-213 |
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| Übergeordnetes Werk: |
volume:18 ; year:2021 ; number:1 ; day:05 ; month:08 ; pages:198-213 |
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| DOI / URN: |
10.1007/s12015-021-10216-9 |
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| 520 | |a Cancer stem cells (CSCs) are rare populations of malignant cells with stem cell-like features of self-renewal, uninterrupted differentiation, tumorigenicity, and resistance to conventional therapeutic agents, and these cells have a decisive role in treatment failure and tumor relapse. The self-renewal potential of CSCs with atypical activation of developmental signaling pathways involves the maintenance of stemness to support cancer progression. The acquisition of stemness in CSCs has been accomplished through genetic and epigenetic rewiring following the metabolic switch. In this context, “metabostemness” denotes the metabolic parameters that essentially govern the epitranscriptional gene reprogramming mechanism to dedifferentiate tumor cells into CSCs. Several metabolites often referred to as oncometabolites can directly remodel chromatin structure and thereby influence the operation of epitranscriptional circuits. This integrated metaboloepigenetic dimension of CSCs favors the differentiated cells to move in dedifferentiated macrostates. Some metabolic events might perform as early drivers of epitranscriptional reprogramming; however, subsequent metabolic hits may govern the retention of stemness properties in the tumor mass. Interestingly, selective removal of mitochondria through autophagy can promote metabolic plasticity and alter metabolic states during differentiation and dedifferentiation. In this connection, novel metabostemness-specific drugs can be generated as potential cancer therapeutics to target the metaboloepigenetic circuitry to eliminate CSCs. Graphical abstract | ||
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10.1007/s12015-021-10216-9 doi (DE-627)SPR046084517 (SPR)s12015-021-10216-9-e DE-627 ger DE-627 rakwb eng Naik, Prajna Paramita verfasserin aut Metabostemness in cancer: Linking metaboloepigenetics and mitophagy in remodeling cancer stem cells 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021 Cancer stem cells (CSCs) are rare populations of malignant cells with stem cell-like features of self-renewal, uninterrupted differentiation, tumorigenicity, and resistance to conventional therapeutic agents, and these cells have a decisive role in treatment failure and tumor relapse. The self-renewal potential of CSCs with atypical activation of developmental signaling pathways involves the maintenance of stemness to support cancer progression. The acquisition of stemness in CSCs has been accomplished through genetic and epigenetic rewiring following the metabolic switch. In this context, “metabostemness” denotes the metabolic parameters that essentially govern the epitranscriptional gene reprogramming mechanism to dedifferentiate tumor cells into CSCs. Several metabolites often referred to as oncometabolites can directly remodel chromatin structure and thereby influence the operation of epitranscriptional circuits. This integrated metaboloepigenetic dimension of CSCs favors the differentiated cells to move in dedifferentiated macrostates. Some metabolic events might perform as early drivers of epitranscriptional reprogramming; however, subsequent metabolic hits may govern the retention of stemness properties in the tumor mass. Interestingly, selective removal of mitochondria through autophagy can promote metabolic plasticity and alter metabolic states during differentiation and dedifferentiation. In this connection, novel metabostemness-specific drugs can be generated as potential cancer therapeutics to target the metaboloepigenetic circuitry to eliminate CSCs. Graphical abstract Cancer Stem Cell (dpeaa)DE-He213 Metaboloepigenetics (dpeaa)DE-He213 Metabostemness (dpeaa)DE-He213 Mitophagy (dpeaa)DE-He213 Oncometabolism (dpeaa)DE-He213 Panigrahi, Swagatika aut Parida, Ratnakar aut Praharaj, Prakash Priyadarshi aut Bhol, Chandra Sekhar aut Patil, Shankargouda aut Manjunath, NML aut Ghosh, Dipanjan aut Patra, Samir Kumar aut Bhutia, Sujit Kumar (orcid)0000-0003-0962-3354 aut Enthalten in Stem cell reviews New York, NY : Springer, 2005 18(2021), 1 vom: 05. Aug., Seite 198-213 (DE-627)494833777 (DE-600)2197218-7 1558-6804 nnns volume:18 year:2021 number:1 day:05 month:08 pages:198-213 https://dx.doi.org/10.1007/s12015-021-10216-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA 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_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_120 GBV_ILN_138 GBV_ILN_152 GBV_ILN_161 GBV_ILN_171 GBV_ILN_187 GBV_ILN_224 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2005 AR 18 2021 1 05 08 198-213 |
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10.1007/s12015-021-10216-9 doi (DE-627)SPR046084517 (SPR)s12015-021-10216-9-e DE-627 ger DE-627 rakwb eng Naik, Prajna Paramita verfasserin aut Metabostemness in cancer: Linking metaboloepigenetics and mitophagy in remodeling cancer stem cells 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021 Cancer stem cells (CSCs) are rare populations of malignant cells with stem cell-like features of self-renewal, uninterrupted differentiation, tumorigenicity, and resistance to conventional therapeutic agents, and these cells have a decisive role in treatment failure and tumor relapse. The self-renewal potential of CSCs with atypical activation of developmental signaling pathways involves the maintenance of stemness to support cancer progression. The acquisition of stemness in CSCs has been accomplished through genetic and epigenetic rewiring following the metabolic switch. In this context, “metabostemness” denotes the metabolic parameters that essentially govern the epitranscriptional gene reprogramming mechanism to dedifferentiate tumor cells into CSCs. Several metabolites often referred to as oncometabolites can directly remodel chromatin structure and thereby influence the operation of epitranscriptional circuits. This integrated metaboloepigenetic dimension of CSCs favors the differentiated cells to move in dedifferentiated macrostates. Some metabolic events might perform as early drivers of epitranscriptional reprogramming; however, subsequent metabolic hits may govern the retention of stemness properties in the tumor mass. Interestingly, selective removal of mitochondria through autophagy can promote metabolic plasticity and alter metabolic states during differentiation and dedifferentiation. In this connection, novel metabostemness-specific drugs can be generated as potential cancer therapeutics to target the metaboloepigenetic circuitry to eliminate CSCs. Graphical abstract Cancer Stem Cell (dpeaa)DE-He213 Metaboloepigenetics (dpeaa)DE-He213 Metabostemness (dpeaa)DE-He213 Mitophagy (dpeaa)DE-He213 Oncometabolism (dpeaa)DE-He213 Panigrahi, Swagatika aut Parida, Ratnakar aut Praharaj, Prakash Priyadarshi aut Bhol, Chandra Sekhar aut Patil, Shankargouda aut Manjunath, NML aut Ghosh, Dipanjan aut Patra, Samir Kumar aut Bhutia, Sujit Kumar (orcid)0000-0003-0962-3354 aut Enthalten in Stem cell reviews New York, NY : Springer, 2005 18(2021), 1 vom: 05. Aug., Seite 198-213 (DE-627)494833777 (DE-600)2197218-7 1558-6804 nnns volume:18 year:2021 number:1 day:05 month:08 pages:198-213 https://dx.doi.org/10.1007/s12015-021-10216-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA 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_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_120 GBV_ILN_138 GBV_ILN_152 GBV_ILN_161 GBV_ILN_171 GBV_ILN_187 GBV_ILN_224 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2005 AR 18 2021 1 05 08 198-213 |
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10.1007/s12015-021-10216-9 doi (DE-627)SPR046084517 (SPR)s12015-021-10216-9-e DE-627 ger DE-627 rakwb eng Naik, Prajna Paramita verfasserin aut Metabostemness in cancer: Linking metaboloepigenetics and mitophagy in remodeling cancer stem cells 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021 Cancer stem cells (CSCs) are rare populations of malignant cells with stem cell-like features of self-renewal, uninterrupted differentiation, tumorigenicity, and resistance to conventional therapeutic agents, and these cells have a decisive role in treatment failure and tumor relapse. The self-renewal potential of CSCs with atypical activation of developmental signaling pathways involves the maintenance of stemness to support cancer progression. The acquisition of stemness in CSCs has been accomplished through genetic and epigenetic rewiring following the metabolic switch. In this context, “metabostemness” denotes the metabolic parameters that essentially govern the epitranscriptional gene reprogramming mechanism to dedifferentiate tumor cells into CSCs. Several metabolites often referred to as oncometabolites can directly remodel chromatin structure and thereby influence the operation of epitranscriptional circuits. This integrated metaboloepigenetic dimension of CSCs favors the differentiated cells to move in dedifferentiated macrostates. Some metabolic events might perform as early drivers of epitranscriptional reprogramming; however, subsequent metabolic hits may govern the retention of stemness properties in the tumor mass. Interestingly, selective removal of mitochondria through autophagy can promote metabolic plasticity and alter metabolic states during differentiation and dedifferentiation. In this connection, novel metabostemness-specific drugs can be generated as potential cancer therapeutics to target the metaboloepigenetic circuitry to eliminate CSCs. Graphical abstract Cancer Stem Cell (dpeaa)DE-He213 Metaboloepigenetics (dpeaa)DE-He213 Metabostemness (dpeaa)DE-He213 Mitophagy (dpeaa)DE-He213 Oncometabolism (dpeaa)DE-He213 Panigrahi, Swagatika aut Parida, Ratnakar aut Praharaj, Prakash Priyadarshi aut Bhol, Chandra Sekhar aut Patil, Shankargouda aut Manjunath, NML aut Ghosh, Dipanjan aut Patra, Samir Kumar aut Bhutia, Sujit Kumar (orcid)0000-0003-0962-3354 aut Enthalten in Stem cell reviews New York, NY : Springer, 2005 18(2021), 1 vom: 05. Aug., Seite 198-213 (DE-627)494833777 (DE-600)2197218-7 1558-6804 nnns volume:18 year:2021 number:1 day:05 month:08 pages:198-213 https://dx.doi.org/10.1007/s12015-021-10216-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA 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_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_120 GBV_ILN_138 GBV_ILN_152 GBV_ILN_161 GBV_ILN_171 GBV_ILN_187 GBV_ILN_224 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2005 AR 18 2021 1 05 08 198-213 |
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10.1007/s12015-021-10216-9 doi (DE-627)SPR046084517 (SPR)s12015-021-10216-9-e DE-627 ger DE-627 rakwb eng Naik, Prajna Paramita verfasserin aut Metabostemness in cancer: Linking metaboloepigenetics and mitophagy in remodeling cancer stem cells 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021 Cancer stem cells (CSCs) are rare populations of malignant cells with stem cell-like features of self-renewal, uninterrupted differentiation, tumorigenicity, and resistance to conventional therapeutic agents, and these cells have a decisive role in treatment failure and tumor relapse. The self-renewal potential of CSCs with atypical activation of developmental signaling pathways involves the maintenance of stemness to support cancer progression. The acquisition of stemness in CSCs has been accomplished through genetic and epigenetic rewiring following the metabolic switch. In this context, “metabostemness” denotes the metabolic parameters that essentially govern the epitranscriptional gene reprogramming mechanism to dedifferentiate tumor cells into CSCs. Several metabolites often referred to as oncometabolites can directly remodel chromatin structure and thereby influence the operation of epitranscriptional circuits. This integrated metaboloepigenetic dimension of CSCs favors the differentiated cells to move in dedifferentiated macrostates. Some metabolic events might perform as early drivers of epitranscriptional reprogramming; however, subsequent metabolic hits may govern the retention of stemness properties in the tumor mass. Interestingly, selective removal of mitochondria through autophagy can promote metabolic plasticity and alter metabolic states during differentiation and dedifferentiation. In this connection, novel metabostemness-specific drugs can be generated as potential cancer therapeutics to target the metaboloepigenetic circuitry to eliminate CSCs. Graphical abstract Cancer Stem Cell (dpeaa)DE-He213 Metaboloepigenetics (dpeaa)DE-He213 Metabostemness (dpeaa)DE-He213 Mitophagy (dpeaa)DE-He213 Oncometabolism (dpeaa)DE-He213 Panigrahi, Swagatika aut Parida, Ratnakar aut Praharaj, Prakash Priyadarshi aut Bhol, Chandra Sekhar aut Patil, Shankargouda aut Manjunath, NML aut Ghosh, Dipanjan aut Patra, Samir Kumar aut Bhutia, Sujit Kumar (orcid)0000-0003-0962-3354 aut Enthalten in Stem cell reviews New York, NY : Springer, 2005 18(2021), 1 vom: 05. Aug., Seite 198-213 (DE-627)494833777 (DE-600)2197218-7 1558-6804 nnns volume:18 year:2021 number:1 day:05 month:08 pages:198-213 https://dx.doi.org/10.1007/s12015-021-10216-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA 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_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_120 GBV_ILN_138 GBV_ILN_152 GBV_ILN_161 GBV_ILN_171 GBV_ILN_187 GBV_ILN_224 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2005 AR 18 2021 1 05 08 198-213 |
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10.1007/s12015-021-10216-9 doi (DE-627)SPR046084517 (SPR)s12015-021-10216-9-e DE-627 ger DE-627 rakwb eng Naik, Prajna Paramita verfasserin aut Metabostemness in cancer: Linking metaboloepigenetics and mitophagy in remodeling cancer stem cells 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021 Cancer stem cells (CSCs) are rare populations of malignant cells with stem cell-like features of self-renewal, uninterrupted differentiation, tumorigenicity, and resistance to conventional therapeutic agents, and these cells have a decisive role in treatment failure and tumor relapse. The self-renewal potential of CSCs with atypical activation of developmental signaling pathways involves the maintenance of stemness to support cancer progression. The acquisition of stemness in CSCs has been accomplished through genetic and epigenetic rewiring following the metabolic switch. In this context, “metabostemness” denotes the metabolic parameters that essentially govern the epitranscriptional gene reprogramming mechanism to dedifferentiate tumor cells into CSCs. Several metabolites often referred to as oncometabolites can directly remodel chromatin structure and thereby influence the operation of epitranscriptional circuits. This integrated metaboloepigenetic dimension of CSCs favors the differentiated cells to move in dedifferentiated macrostates. Some metabolic events might perform as early drivers of epitranscriptional reprogramming; however, subsequent metabolic hits may govern the retention of stemness properties in the tumor mass. Interestingly, selective removal of mitochondria through autophagy can promote metabolic plasticity and alter metabolic states during differentiation and dedifferentiation. In this connection, novel metabostemness-specific drugs can be generated as potential cancer therapeutics to target the metaboloepigenetic circuitry to eliminate CSCs. Graphical abstract Cancer Stem Cell (dpeaa)DE-He213 Metaboloepigenetics (dpeaa)DE-He213 Metabostemness (dpeaa)DE-He213 Mitophagy (dpeaa)DE-He213 Oncometabolism (dpeaa)DE-He213 Panigrahi, Swagatika aut Parida, Ratnakar aut Praharaj, Prakash Priyadarshi aut Bhol, Chandra Sekhar aut Patil, Shankargouda aut Manjunath, NML aut Ghosh, Dipanjan aut Patra, Samir Kumar aut Bhutia, Sujit Kumar (orcid)0000-0003-0962-3354 aut Enthalten in Stem cell reviews New York, NY : Springer, 2005 18(2021), 1 vom: 05. Aug., Seite 198-213 (DE-627)494833777 (DE-600)2197218-7 1558-6804 nnns volume:18 year:2021 number:1 day:05 month:08 pages:198-213 https://dx.doi.org/10.1007/s12015-021-10216-9 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA 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_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_120 GBV_ILN_138 GBV_ILN_152 GBV_ILN_161 GBV_ILN_171 GBV_ILN_187 GBV_ILN_224 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2005 AR 18 2021 1 05 08 198-213 |
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Naik, Prajna Paramita Panigrahi, Swagatika Parida, Ratnakar Praharaj, Prakash Priyadarshi Bhol, Chandra Sekhar Patil, Shankargouda Manjunath, NML Ghosh, Dipanjan Patra, Samir Kumar Bhutia, Sujit Kumar |
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Metabostemness in cancer: Linking metaboloepigenetics and mitophagy in remodeling cancer stem cells |
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Cancer stem cells (CSCs) are rare populations of malignant cells with stem cell-like features of self-renewal, uninterrupted differentiation, tumorigenicity, and resistance to conventional therapeutic agents, and these cells have a decisive role in treatment failure and tumor relapse. The self-renewal potential of CSCs with atypical activation of developmental signaling pathways involves the maintenance of stemness to support cancer progression. The acquisition of stemness in CSCs has been accomplished through genetic and epigenetic rewiring following the metabolic switch. In this context, “metabostemness” denotes the metabolic parameters that essentially govern the epitranscriptional gene reprogramming mechanism to dedifferentiate tumor cells into CSCs. Several metabolites often referred to as oncometabolites can directly remodel chromatin structure and thereby influence the operation of epitranscriptional circuits. This integrated metaboloepigenetic dimension of CSCs favors the differentiated cells to move in dedifferentiated macrostates. Some metabolic events might perform as early drivers of epitranscriptional reprogramming; however, subsequent metabolic hits may govern the retention of stemness properties in the tumor mass. Interestingly, selective removal of mitochondria through autophagy can promote metabolic plasticity and alter metabolic states during differentiation and dedifferentiation. In this connection, novel metabostemness-specific drugs can be generated as potential cancer therapeutics to target the metaboloepigenetic circuitry to eliminate CSCs. Graphical abstract © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021 |
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Cancer stem cells (CSCs) are rare populations of malignant cells with stem cell-like features of self-renewal, uninterrupted differentiation, tumorigenicity, and resistance to conventional therapeutic agents, and these cells have a decisive role in treatment failure and tumor relapse. The self-renewal potential of CSCs with atypical activation of developmental signaling pathways involves the maintenance of stemness to support cancer progression. The acquisition of stemness in CSCs has been accomplished through genetic and epigenetic rewiring following the metabolic switch. In this context, “metabostemness” denotes the metabolic parameters that essentially govern the epitranscriptional gene reprogramming mechanism to dedifferentiate tumor cells into CSCs. Several metabolites often referred to as oncometabolites can directly remodel chromatin structure and thereby influence the operation of epitranscriptional circuits. This integrated metaboloepigenetic dimension of CSCs favors the differentiated cells to move in dedifferentiated macrostates. Some metabolic events might perform as early drivers of epitranscriptional reprogramming; however, subsequent metabolic hits may govern the retention of stemness properties in the tumor mass. Interestingly, selective removal of mitochondria through autophagy can promote metabolic plasticity and alter metabolic states during differentiation and dedifferentiation. In this connection, novel metabostemness-specific drugs can be generated as potential cancer therapeutics to target the metaboloepigenetic circuitry to eliminate CSCs. Graphical abstract © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021 |
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Cancer stem cells (CSCs) are rare populations of malignant cells with stem cell-like features of self-renewal, uninterrupted differentiation, tumorigenicity, and resistance to conventional therapeutic agents, and these cells have a decisive role in treatment failure and tumor relapse. The self-renewal potential of CSCs with atypical activation of developmental signaling pathways involves the maintenance of stemness to support cancer progression. The acquisition of stemness in CSCs has been accomplished through genetic and epigenetic rewiring following the metabolic switch. In this context, “metabostemness” denotes the metabolic parameters that essentially govern the epitranscriptional gene reprogramming mechanism to dedifferentiate tumor cells into CSCs. Several metabolites often referred to as oncometabolites can directly remodel chromatin structure and thereby influence the operation of epitranscriptional circuits. This integrated metaboloepigenetic dimension of CSCs favors the differentiated cells to move in dedifferentiated macrostates. Some metabolic events might perform as early drivers of epitranscriptional reprogramming; however, subsequent metabolic hits may govern the retention of stemness properties in the tumor mass. Interestingly, selective removal of mitochondria through autophagy can promote metabolic plasticity and alter metabolic states during differentiation and dedifferentiation. In this connection, novel metabostemness-specific drugs can be generated as potential cancer therapeutics to target the metaboloepigenetic circuitry to eliminate CSCs. Graphical abstract © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021 |
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Interestingly, selective removal of mitochondria through autophagy can promote metabolic plasticity and alter metabolic states during differentiation and dedifferentiation. In this connection, novel metabostemness-specific drugs can be generated as potential cancer therapeutics to target the metaboloepigenetic circuitry to eliminate CSCs. 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