Epigenetic regulation of cancer stemness
Abstract Gene expression is finely controlled by the abundance and activation status of transcription factors and their regulators, as well as by a number of reversible modifications of DNA and histones that are commonly referred to as epigenetic marks. Such alterations (i.e., methylation, acetylati...
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| Format: | Article |
| Language: | English |
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Nature Publishing Group
2025-08-01
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| Series: | Signal Transduction and Targeted Therapy |
| Online Access: | https://doi.org/10.1038/s41392-025-02340-6 |
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| author | Claudia Galassi Gwenola Manic Manel Esteller Lorenzo Galluzzi Ilio Vitale |
| author_facet | Claudia Galassi Gwenola Manic Manel Esteller Lorenzo Galluzzi Ilio Vitale |
| author_sort | Claudia Galassi |
| collection | DOAJ |
| description | Abstract Gene expression is finely controlled by the abundance and activation status of transcription factors and their regulators, as well as by a number of reversible modifications of DNA and histones that are commonly referred to as epigenetic marks. Such alterations (i.e., methylation, acetylation, and ubiquitination) are catalyzed by an array of dedicated enzymes with antagonistic activity, including methyltransferases and demethylases, acetyltransferases and deacetylases, as well as ubiquitin ligases and deubiquitinating enzymes. The epigenetic control of transcription is critical not only for embryonic and postembryonic development but also for the preservation of homeostasis in all adult tissues. In line with this notion, epigenetic defects have been associated with a variety of human disorders, including (but not limited to) congenital conditions as well as multiple hematological and solid tumors. Here, we provide an in-depth discussion of the impact of epigenetic alterations on cancer stemness, i.e., the ability of a small population of poorly differentiated malignant cells to (1) self-renew while generating a more differentiated progeny, and (2) exhibit superior tumor initiating/repopulating potential along with exceptional plasticity and improved resistance to environmental and therapy-elicited stress. Moreover, we critically evaluate the potential and limitations of targeting epigenetic modifiers as a means to eradicate cancer stem cells for therapeutic purposes. |
| format | Article |
| id | doaj-art-63f48ecec39a4298a2513f60ba9d08d1 |
| institution | DOAJ |
| issn | 2059-3635 |
| language | English |
| publishDate | 2025-08-01 |
| publisher | Nature Publishing Group |
| record_format | Article |
| series | Signal Transduction and Targeted Therapy |
| spelling | doaj-art-63f48ecec39a4298a2513f60ba9d08d12025-08-20T03:06:09ZengNature Publishing GroupSignal Transduction and Targeted Therapy2059-36352025-08-0110111910.1038/s41392-025-02340-6Epigenetic regulation of cancer stemnessClaudia Galassi0Gwenola Manic1Manel Esteller2Lorenzo Galluzzi3Ilio Vitale4Department of Pharmacology, Weill Cornell Medical CollegeItalian Institute for Genomic Medicine, c/o IRCSS CandioloCancer Epigenetics Group, Josep Carreras Leukemia Research Institute (IJC)Cancer Signaling and Microenvironment Program, Fox Chase Cancer CenterItalian Institute for Genomic Medicine, c/o IRCSS CandioloAbstract Gene expression is finely controlled by the abundance and activation status of transcription factors and their regulators, as well as by a number of reversible modifications of DNA and histones that are commonly referred to as epigenetic marks. Such alterations (i.e., methylation, acetylation, and ubiquitination) are catalyzed by an array of dedicated enzymes with antagonistic activity, including methyltransferases and demethylases, acetyltransferases and deacetylases, as well as ubiquitin ligases and deubiquitinating enzymes. The epigenetic control of transcription is critical not only for embryonic and postembryonic development but also for the preservation of homeostasis in all adult tissues. In line with this notion, epigenetic defects have been associated with a variety of human disorders, including (but not limited to) congenital conditions as well as multiple hematological and solid tumors. Here, we provide an in-depth discussion of the impact of epigenetic alterations on cancer stemness, i.e., the ability of a small population of poorly differentiated malignant cells to (1) self-renew while generating a more differentiated progeny, and (2) exhibit superior tumor initiating/repopulating potential along with exceptional plasticity and improved resistance to environmental and therapy-elicited stress. Moreover, we critically evaluate the potential and limitations of targeting epigenetic modifiers as a means to eradicate cancer stem cells for therapeutic purposes.https://doi.org/10.1038/s41392-025-02340-6 |
| spellingShingle | Claudia Galassi Gwenola Manic Manel Esteller Lorenzo Galluzzi Ilio Vitale Epigenetic regulation of cancer stemness Signal Transduction and Targeted Therapy |
| title | Epigenetic regulation of cancer stemness |
| title_full | Epigenetic regulation of cancer stemness |
| title_fullStr | Epigenetic regulation of cancer stemness |
| title_full_unstemmed | Epigenetic regulation of cancer stemness |
| title_short | Epigenetic regulation of cancer stemness |
| title_sort | epigenetic regulation of cancer stemness |
| url | https://doi.org/10.1038/s41392-025-02340-6 |
| work_keys_str_mv | AT claudiagalassi epigeneticregulationofcancerstemness AT gwenolamanic epigeneticregulationofcancerstemness AT manelesteller epigeneticregulationofcancerstemness AT lorenzogalluzzi epigeneticregulationofcancerstemness AT iliovitale epigeneticregulationofcancerstemness |