ArticleDevelopmental cell2025
Sumoylated Etv1 establishes mouse mammary cancer stem cells that support tumorigenesis by non-stem cancer cells.
Article in Developmental cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- PML-driven sumoylation of PML::RARA-bound repressors drives hematopoietic progenitor immortalization.The Journal of experimental medicine · 2026Article
- Small modifier, big decision: switching to SUMO mode adds weight to cancer stemness in mammary tumors.Molecular oncology · 2025Article
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
The small ubiquitin-like modifier (SUMO) pathway is required for maintenance of cancer stem cells/tumor-initiating cells (CSCs/TICs), which drive tumorigenesis when transplanted into immunocompromised mice. We found that inhibition of the SUMO pathway blocked Neu-mediated mammary oncogenesis and inhibited the function of CSCs/TICs without effects on normal mammary stem cells. Transcriptomic analysis implicated SUMO-conjugated Etv1 as being critical for oncogenesis. After SUMO pathway inhibition, a SUMO-mimetic Etv1 protein, created by a fusion with SUMO1 or SUMO2, established a stem-like cell capable of tumorigenesis, whereas a SUMO-resistant Etv1 protein established a proliferative, non-tumorigenic cell. In mixing experiments, stem-like cells induced tumorigenesis by non-stem cells. We conclude that SUMO-conjugated Etv1 is necessary to maintain the CSC/TIC phenotype and that crosstalk between stem and non-stem cells is crucial for tumorigenesis. The findings demonstrate dynamic interactions between heterogeneous cell types to drive tumorigenesis, which has implications for future cancer therapeutic development.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.