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<p>Glioblastoma multiforme (GBM) is a highly aggressive brain tumor with limited treatment options and a poor prognosis. Its defining features include rapid proliferation, invasive capacity, and resistance to therapy. Bioinformatics analyses using TCGA and UALCAN datasets were conducted to assess MXRA8 and ELF3 expression and their association with patient survival. The expression levels were validated through qPCR and western blotting. Functional assays, including proliferation, migration, and invasion tests, were performed after silencing or overexpressing MXRA8 and ELF3. Chromatin immunoprecipitation (ChIP) and dual-luciferase reporter assays determined ELF3’s role in regulating MXRA8 transcription. An in vivo xenograft model was used to evaluate the effects of ELF3 and MXRA8 on tumor growth. MXRA8 expression was significantly elevated in GBM tissues and associated with reduced overall survival. Functional analyses revealed that MXRA8 knockdown inhibited oncogenic traits. Moreover, ELF3 was overexpressed in GBM tissues and positively correlated with MXRA8 expression. ChIP and dual-luciferase assays confirmed that ELF3 binds to the MXRA8 promoter and activates its transcription. Rescue experiments showed that MXRA8 overexpression could reverse the tumor-suppressive effects of ELF3 knockdown. In vivo, silencing ELF3 or MXRA8 inhibited tumor growth and proliferation. This study suggests that the ELF3-MXRA8 axis may be a critical driver of GBM progression, with ELF3 promoting tumor growth and invasion through transcriptional activation of MXRA8.</p>

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ELF3 drives glioblastoma multiforme progression through the regulation of MXRA8 expression

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月1日

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  • Maomao Wang,
  • Haiji Bo,
  • Dapeng Chen,
  • Jiangxin Mao,
  • Zong Miao,
  • Laixing Wang

摘要

Glioblastoma multiforme (GBM) is a highly aggressive brain tumor with limited treatment options and a poor prognosis. Its defining features include rapid proliferation, invasive capacity, and resistance to therapy. Bioinformatics analyses using TCGA and UALCAN datasets were conducted to assess MXRA8 and ELF3 expression and their association with patient survival. The expression levels were validated through qPCR and western blotting. Functional assays, including proliferation, migration, and invasion tests, were performed after silencing or overexpressing MXRA8 and ELF3. Chromatin immunoprecipitation (ChIP) and dual-luciferase reporter assays determined ELF3’s role in regulating MXRA8 transcription. An in vivo xenograft model was used to evaluate the effects of ELF3 and MXRA8 on tumor growth. MXRA8 expression was significantly elevated in GBM tissues and associated with reduced overall survival. Functional analyses revealed that MXRA8 knockdown inhibited oncogenic traits. Moreover, ELF3 was overexpressed in GBM tissues and positively correlated with MXRA8 expression. ChIP and dual-luciferase assays confirmed that ELF3 binds to the MXRA8 promoter and activates its transcription. Rescue experiments showed that MXRA8 overexpression could reverse the tumor-suppressive effects of ELF3 knockdown. In vivo, silencing ELF3 or MXRA8 inhibited tumor growth and proliferation. This study suggests that the ELF3-MXRA8 axis may be a critical driver of GBM progression, with ELF3 promoting tumor growth and invasion through transcriptional activation of MXRA8.