Nucleoli-localized KANSL2 as an epigenetic regulator of ribosome biogenesis in glioblastoma cells
Summary
KANSL2 is a subunit of the non-specific lethal (NSL) chromatin-modifying complex associated with glioblastoma (GBM) progression, but the intrinsic role of KANSL2 in GBM cells is poorly understood. By analyzing TCGA-GBM and GTEx datasets, we found that KANSL2 is upregulated in GBM and positively correlates with genes involved in ribosome biogenesis. Immunofluorescence and cell cycle analyses reveal a dynamic nuclear distribution, with KANSL2 becoming enriched in nucleoli mainly during G1/early S and G2 phases. Overexpression of KANSL2 increases 45S pre-rRNA and 28S rRNA levels, whereas its silencing reduces rRNA expression and histone H4 acetylation at lysines 5 and 8 within rDNA promoters. RNA-seq of patient-derived GBM spheroids confirms a global downregulation of ribosome biogenesis genes upon silencing of KANSL2. Together, these findings identify KANSL2 as a nuclear factor that transiently associates with nucleoli to promote rRNA transcription and ribosome biogenesis, supporting the biosynthetic and proliferative capacity of glioblastoma cells. © 2026. The Author(s).
| Authors | Budnik N, Canedo L, Morellato AE, Cuenca MB, Garmendia M, Senin S, Romano SA, Andrysik Z, Videla-Richardson GA, Graner MW, Kobayashi K, Zhou Y, Wiese M, Akhtar A, Espinosa JM, Perez-Castro C |
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| Journal | Communications biology |
| Publication Date | 2026 Mar 5;9(1) |
| PubMed | 41787092 |
| PubMed Central | PMC13086876 |
| DOI | 10.1038/s42003-026-09808-3 |