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<p>Glioblastoma (GBM) is one of the most malignant primary brain tumors, and factors governing its progression are not fully characterized. Recent research suggests that the long non-coding RNA (lncRNA) HOTAIR and super-enhancers (SEs) contribute significantly to GBM progression. Here, we performed TCGA data analysis revealing that high HOTAIR expression in GBM is associated with poor prognosis. Conversely, HOTAIR knock-down (KD) decreased proliferation, colony formation, and invasion of GBM cells. Furthermore, RNA-seq analysis identified DEGs in GBM cells related to cell growth and adhesion. Using an integrated approach, we also identify <i>MEST</i> as a HOTAIR-associated SE target gene. Intriguingly, <i>MEST</i> suppression in GBM cells phenocopied HOTAIR KD, as evidenced by reduced cell proliferation and invasion, whereas MEST overexpression counteracted effects of HOTAIR depletion. Moreover, 3 C technique-based PCR confirmed reduced interaction between HOTAIR-associated SEs and target genes after HOTAIR KD. This study reveals a novel regulatory mechanism governing GBM, offering promising directions for clinical interventions.</p>

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A HOTAIR-associated super-enhancer orchestrates glioblastoma malignancy via MEST

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年4月7日

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  • Peng Li,
  • Yang Yang,
  • Chunpeng Luan,
  • Wenbin Wang,
  • Yuan Jiang,
  • Zhenhao Zhao,
  • Bo Wang,
  • Yuting Zhao,
  • Yunlong Bai,
  • Man Liu,
  • Zhongfang Zhao,
  • Lei Zhang,
  • Yuyang Qian,
  • Jiandang Shi

摘要

Glioblastoma (GBM) is one of the most malignant primary brain tumors, and factors governing its progression are not fully characterized. Recent research suggests that the long non-coding RNA (lncRNA) HOTAIR and super-enhancers (SEs) contribute significantly to GBM progression. Here, we performed TCGA data analysis revealing that high HOTAIR expression in GBM is associated with poor prognosis. Conversely, HOTAIR knock-down (KD) decreased proliferation, colony formation, and invasion of GBM cells. Furthermore, RNA-seq analysis identified DEGs in GBM cells related to cell growth and adhesion. Using an integrated approach, we also identify MEST as a HOTAIR-associated SE target gene. Intriguingly, MEST suppression in GBM cells phenocopied HOTAIR KD, as evidenced by reduced cell proliferation and invasion, whereas MEST overexpression counteracted effects of HOTAIR depletion. Moreover, 3 C technique-based PCR confirmed reduced interaction between HOTAIR-associated SEs and target genes after HOTAIR KD. This study reveals a novel regulatory mechanism governing GBM, offering promising directions for clinical interventions.