Small modifier, big decision: switching to SUMO mode adds weight to cancer stemness in mammary tumors

Protein SUMOylation is crucial for maintaining the hallmarks of cancer stem cells, including self‐renewal and active pluripotency gene networks. While inhibiting key steps of the SUMOylation cascade has been shown to suppress tumorigenesis, the specific mechanisms of SUMO dependency in cancer have n...

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Published in:	Molecular oncology Vol. 19; no. 8; pp. 2166 - 2170
Main Authors:	Yevdokimova, Veronika, Benoit, Yannick D.
Format:	Journal Article
Language:	English
Published:	United States John Wiley & Sons, Inc 01.08.2025 John Wiley and Sons Inc Wiley
Subjects:	Animals B cells Breast cancer Breast Neoplasms - metabolism Breast Neoplasms - pathology Cancer Cancer and Oncology Cancer Stem Cells chromatin regulation Colorectal cancer drug discovery Enzymes Female Genetic engineering Genetically modified organisms Humans Leukemia Lymphoma Mammary gland Medical research Neoplastic Stem Cells - metabolism Neoplastic Stem Cells - pathology Pancreatic cancer Pluripotency Proteases Small Ubiquitin-Related Modifier Proteins - metabolism Stem cells SUMO protein SUMOylation Transcription factors Transcription Factors - metabolism Tumorigenesis Tumors breast cancer SUMOylation cancer stem cells drug discovery chromatin regulation
ISSN:	1574-7891, 1878-0261, 1878-0261
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Abstract	Protein SUMOylation is crucial for maintaining the hallmarks of cancer stem cells, including self‐renewal and active pluripotency gene networks. While inhibiting key steps of the SUMOylation cascade has been shown to suppress tumorigenesis, the specific mechanisms of SUMO dependency in cancer have not been comprehensively characterized. Li et al. applied genetically engineered models of mammary gland tumorigenesis to demonstrate that SUMOylation of the transcription factor Etv1 is essential for maintaining cancer stem cell functions. Moreover, SUMO conjugation of Etv1 acts as a switch between stem and nonstem cancer cell states. Here, we discuss the implications of these findings regarding the role of SUMOylation‐dependent mechanisms in the hierarchical organization of malignant cells and intratumor heterogeneity and highlight potential therapeutic approaches harnessing the SUMOylation cascade. Inhibition of protein SUMOylation has been shown to block tumorigenesis; however, the specific mechanisms by which SUMOylation controls the tumor‐initiating capacities remain elusive. Li et al. describe the role of Etv1 SUMOylation in cancer stem cells using mouse models of mammary gland tumorigenesis. Here, we discuss the implications of these findings and highlight potential anticancer therapeutic approaches targeting this cascade.
AbstractList	Protein SUMOylation is crucial for maintaining the hallmarks of cancer stem cells, including self-renewal and active pluripotency gene networks. While inhibiting key steps of the SUMOylation cascade has been shown to suppress tumorigenesis, the specific mechanisms of SUMO dependency in cancer have not been comprehensively characterized. Li et al. applied genetically engineered models of mammary gland tumorigenesis to demonstrate that SUMOylation of the transcription factor Etv1 is essential for maintaining cancer stem cell functions. Moreover, SUMO conjugation of Etv1 acts as a switch between stem and nonstem cancer cell states. Here, we discuss the implications of these findings regarding the role of SUMOylation-dependent mechanisms in the hierarchical organization of malignant cells and intratumor heterogeneity and highlight potential therapeutic approaches harnessing the SUMOylation cascade. Protein SUMOylation is crucial for maintaining the hallmarks of cancer stem cells, including self‐renewal and active pluripotency gene networks. While inhibiting key steps of the SUMOylation cascade has been shown to suppress tumorigenesis, the specific mechanisms of SUMO dependency in cancer have not been comprehensively characterized. Li et al. applied genetically engineered models of mammary gland tumorigenesis to demonstrate that SUMOylation of the transcription factor Etv1 is essential for maintaining cancer stem cell functions. Moreover, SUMO conjugation of Etv1 acts as a switch between stem and nonstem cancer cell states. Here, we discuss the implications of these findings regarding the role of SUMOylation‐dependent mechanisms in the hierarchical organization of malignant cells and intratumor heterogeneity and highlight potential therapeutic approaches harnessing the SUMOylation cascade. Protein SUMOylation is crucial for maintaining the hallmarks of cancer stem cells, including self-renewal and active pluripotency gene networks. While inhibiting key steps of the SUMOylation cascade has been shown to suppress tumorigenesis, the specific mechanisms of SUMO dependency in cancer have not been comprehensively characterized. Li et al. applied genetically engineered models of mammary gland tumorigenesis to demonstrate that SUMOylation of the transcription factor Etv1 is essential for maintaining cancer stem cell functions. Moreover, SUMO conjugation of Etv1 acts as a switch between stem and nonstem cancer cell states. Here, we discuss the implications of these findings regarding the role of SUMOylation-dependent mechanisms in the hierarchical organization of malignant cells and intratumor heterogeneity and highlight potential therapeutic approaches harnessing the SUMOylation cascade.Protein SUMOylation is crucial for maintaining the hallmarks of cancer stem cells, including self-renewal and active pluripotency gene networks. While inhibiting key steps of the SUMOylation cascade has been shown to suppress tumorigenesis, the specific mechanisms of SUMO dependency in cancer have not been comprehensively characterized. Li et al. applied genetically engineered models of mammary gland tumorigenesis to demonstrate that SUMOylation of the transcription factor Etv1 is essential for maintaining cancer stem cell functions. Moreover, SUMO conjugation of Etv1 acts as a switch between stem and nonstem cancer cell states. Here, we discuss the implications of these findings regarding the role of SUMOylation-dependent mechanisms in the hierarchical organization of malignant cells and intratumor heterogeneity and highlight potential therapeutic approaches harnessing the SUMOylation cascade. Protein SUMOylation is crucial for maintaining the hallmarks of cancer stem cells, including self‐renewal and active pluripotency gene networks. While inhibiting key steps of the SUMOylation cascade has been shown to suppress tumorigenesis, the specific mechanisms of SUMO dependency in cancer have not been comprehensively characterized. Li et al. applied genetically engineered models of mammary gland tumorigenesis to demonstrate that SUMOylation of the transcription factor Etv1 is essential for maintaining cancer stem cell functions. Moreover, SUMO conjugation of Etv1 acts as a switch between stem and nonstem cancer cell states. Here, we discuss the implications of these findings regarding the role of SUMOylation‐dependent mechanisms in the hierarchical organization of malignant cells and intratumor heterogeneity and highlight potential therapeutic approaches harnessing the SUMOylation cascade. Inhibition of protein SUMOylation has been shown to block tumorigenesis; however, the specific mechanisms by which SUMOylation controls the tumor‐initiating capacities remain elusive. Li et al. describe the role of Etv1 SUMOylation in cancer stem cells using mouse models of mammary gland tumorigenesis. Here, we discuss the implications of these findings and highlight potential anticancer therapeutic approaches targeting this cascade. Protein SUMOylation is crucial for maintaining the hallmarks of cancer stem cells, including self‐renewal and active pluripotency gene networks. While inhibiting key steps of the SUMOylation cascade has been shown to suppress tumorigenesis, the specific mechanisms of SUMO dependency in cancer have not been comprehensively characterized. Li et al. applied genetically engineered models of mammary gland tumorigenesis to demonstrate that SUMOylation of the transcription factor Etv1 is essential for maintaining cancer stem cell functions. Moreover, SUMO conjugation of Etv1 acts as a switch between stem and nonstem cancer cell states. Here, we discuss the implications of these findings regarding the role of SUMOylation‐dependent mechanisms in the hierarchical organization of malignant cells and intratumor heterogeneity and highlight potential therapeutic approaches harnessing the SUMOylation cascade. Inhibition of protein SUMOylation has been shown to block tumorigenesis; however, the specific mechanisms by which SUMOylation controls the tumor‐initiating capacities remain elusive. Li et al. describe the role of Etv1 SUMOylation in cancer stem cells using mouse models of mammary gland tumorigenesis. Here, we discuss the implications of these findings and highlight potential anticancer therapeutic approaches targeting this cascade.
Audience	Academic
Author	Benoit, Yannick D. Yevdokimova, Veronika
AuthorAffiliation	1 Department of Cellular and Molecular Medicine Faculty of Medicine, University of Ottawa Canada 2 School of Pharmaceutical Sciences Faculty of Medicine, University of Ottawa Canada
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Cites_doi	10.1038/nature09409 10.1038/s43018‐024‐00727‐y 10.1016/j.isci.2021.103442 10.1126/science.1212728 10.3390/cancers13174402 10.1016/j.stem.2018.10.001 10.1158/1535‐7163.MCT‐23‐0572 10.1073/pnas.1818210116 10.1016/j.celrep.2023.112380 10.1016/j.chembiol.2017.05.026 10.1016/j.chembiol.2021.04.014 10.1126/scitranslmed.aba7791 10.1172/JCI152383 10.1038/s41388‐020‐01457‐y 10.1016/j.devcel.2025.04.005 10.1016/j.molcel.2021.11.011
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Copyright	2025 The Author(s). published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies. 2025 The Author(s). Molecular Oncology published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies. COPYRIGHT 2025 John Wiley & Sons, Inc. 2025. This work is published under http://creativecommons.org/licenses/by/4.0/ (the "License"). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
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Snippet	Protein SUMOylation is crucial for maintaining the hallmarks of cancer stem cells, including self‐renewal and active pluripotency gene networks. While... Protein SUMOylation is crucial for maintaining the hallmarks of cancer stem cells, including self-renewal and active pluripotency gene networks. While...
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StartPage	2166
SubjectTerms	Animals B cells Breast cancer Breast Neoplasms - metabolism Breast Neoplasms - pathology Cancer Cancer and Oncology Cancer Stem Cells chromatin regulation Colorectal cancer drug discovery Enzymes Female Genetic engineering Genetically modified organisms Humans Leukemia Lymphoma Mammary gland Medical research Neoplastic Stem Cells - metabolism Neoplastic Stem Cells - pathology Pancreatic cancer Pluripotency Proteases Small Ubiquitin-Related Modifier Proteins - metabolism Stem cells SUMO protein SUMOylation Transcription factors Transcription Factors - metabolism Tumorigenesis Tumors
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Title	Small modifier, big decision: switching to SUMO mode adds weight to cancer stemness in mammary tumors
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