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<p>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.</p>

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Nucleoli-localized KANSL2 as an epigenetic regulator of ribosome biogenesis in glioblastoma cells

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月5日

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  • 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,
  • Ken Kobayashi,
  • Yilong Zhou,
  • Meike Wiese,
  • Asifa Akhtar,
  • Joaquín M. Espinosa,
  • Carolina Perez-Castro

摘要

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.