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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Bibliographic Details
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
Online Access:Get full text
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Summary: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.
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ISSN:1574-7891
1878-0261
1878-0261
DOI:10.1002/1878-0261.70082