ArticleCommunications biology2026
Nucleoli-localized KANSL2 as an epigenetic regulator of ribosome biogenesis in glioblastoma cells.
Nicolás Budnik, Lucía Canedo, Agustín E Morellato, Marina B Cuenca, Martina Garmendia, Sergio Senin, Sebastián A Romano, Zdenek Andrysik, Guillermo A Videla-Richardson, Michael W Graner and 6 more
Abstract read
In one paragraphArticle in Communications biology, 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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2 · The registryThe trial behind it
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4 · The recordCorrections and comments
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5 · Who and what moneyAuthors and funding
16 authors.
Lucía Canedo *Instituto de Investigación en Biomedicina de Buenos Aires (IBioBA) - CONICET -Partner Institute of the Max Planck Society, Buenos Aires, Argentina.
Agustín E MorellatoInstituto de Investigación en Biomedicina de Buenos Aires (IBioBA) - CONICET -Partner Institute of the Max Planck Society, Buenos Aires, Argentina.
Marina B CuencaInstituto de Investigación en Biomedicina de Buenos Aires (IBioBA) - CONICET -Partner Institute of the Max Planck Society, Buenos Aires, Argentina.
Martina GarmendiaInstituto de Investigación en Biomedicina de Buenos Aires (IBioBA) - CONICET -Partner Institute of the Max Planck Society, Buenos Aires, Argentina.
Sergio SeninInstituto de Investigación en Biomedicina de Buenos Aires (IBioBA) - CONICET -Partner Institute of the Max Planck Society, Buenos Aires, Argentina.
Sebastián A RomanoInstituto de Investigación en Biomedicina de Buenos Aires (IBioBA) - CONICET -Partner Institute of the Max Planck Society, Buenos Aires, Argentina.
Zdenek AndrysikLinda Crnic Institute for Down Syndrome, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Guillermo A Videla-RichardsonLaboratorio de Investigación Aplicada a Neurociencias (LIAN). Instituto de Neurociencias (INEU)., Fundación para la Lucha contra las Enfermedades Neurológicas de la Infancia (FLENI)-CONICET, Buenos Aires, Argentina.
Michael W GranerDepartment of Neurosurgery, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Ken KobayashiLaboratorio de Agrobiotecnología, Departamento de Fisiología, Biología Molecular y Celular (FBMC), Instituto de Biodiversidad y Biología Experimental Aplicada (IBBEA-CONICET-UBA), Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Buenos Aires, Argentina.
Carolina Perez-CastroInstituto de Investigación en Biomedicina de Buenos Aires (IBioBA) - CONICET -Partner Institute of the Max Planck Society, Buenos Aires, Argentina. cperezcastro@ibioba-mpsp-conicet.gov.ar.ORCID http://orcid.org/0000-0001-8792-7383 Funding
Ministry of Science, Technology and Productive Innovation, Argentina | Agencia Nacional de Promoción Científica y Tecnológica (National Agency for Science and Technology, Argentina) PICT 2016-4201Ministry of Science, Technology and Productive Innovation, Argentina | Agencia Nacional de Promoción Científica y Tecnológica (National Agency for Science and Technology, Argentina) PICT 2018-02891Ministry of Science, Technology and Productive Innovation, Argentina | Agencia Nacional de Promoción Científica y Tecnológica (National Agency for Science and Technology, Argentina) PICT 2021-0076Ministry of Science, Technology and Productive Innovation, Argentina | Agencia Nacional de Promoción Científica y Tecnológica (National Agency for Science and Technology, Argentina) PICT 2021-I-A-00315
6 · The paper itselfAbstract
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.
Indexed as
Brain NeoplasmsCell NucleolusEpigenesis, GeneticGlioblastomaRibosomesCell Line, TumorGene Expression Regulation, NeoplasticHumansRNA, RibosomalRNA, Ribosomal
Identifiers
PMID41787092
PMCPMC13086876
What OpenQuestion holds
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LicenceCC BY
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