ArticleCancers2026
αS-SETMAR: Inducing Protective Chaos in Glioblastoma?
Article in Cancers, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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Authors and funding
8 authors.
Funding
Abstract
BACKGROUND/
objectivesGlioblastoma remains the most aggressive and lethal form of brain cancer, with no effective cure to date. The molecular mechanisms sustaining its development and relentless proliferation are still not fully understood. SETMAR, a protein lysine methyltransferase involved in various DNA repair and chromatin processes, has been reported as dysregulated in several cancers, including glioblastoma. Interestingly, S-SETMAR, a shorter isoform of SETMAR, has been suggested to antagonize the oncogenic properties of the full-length protein. Here, we explored the cellular and molecular consequences of S-SETMAR overexpression in glioblastoma cells.
methodsWe compared native glioblastoma cells (8MGBA) with a recombinant 8MGBA line stably over-expressing αS-SETMAR, a stable form of S-SETMAR, using complementary cellular and molecular approaches.
resultsOverexpression of αS-SETMAR markedly prolonged the cell cycle duration (from 27 to 37 h), leading to a significant decrease in cell proliferation. Unexpectedly, αS-SETMAR triggered genomic alterations characterized by an increased DNA content and extensive chromosomal instability, including aneuploidy, chromoanasynthesis-like rearrangements, and tripolar mitoses. Moreover, αS-SETMAR-expressing cells displayed heightened sensitivity to stress conditions mimicking chemotherapy and radiotherapy, resulting in increased apoptosis.
conclusionsOur findings identify αS-SETMAR as a dual modulator of glioblastoma cell fate-simultaneously slowing proliferation and promoting chromosomal instability while enhancing vulnerability to genotoxic stress. These results suggest that αS-SETMAR could serve as both a prognostic marker and a potential therapeutic tool in glioblastoma management.
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