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<p>Temozolomide (TMZ) constitutes the first-line chemotherapeutic regimen for glioblastoma (GBM), yet its clinical efficacy remains suboptimal. β-lapachone, a naturally occurring NQO1 inhibitor, has demonstrated potent antitumor activity across multiple malignancies. Based on the critical involvement of nuclear factor-κB (NF-κB) in GBM pathogenesis, this study investigated whether β-lapachone can enhance the antitumor effect of TMZ by targeting the NF-κB pathway using both in vitro and in vivo models. We found that β-lapachone acts synergistically with TMZ to inhibit GBM cell proliferation, epithelial–mesenchymal transition (EMT), and angiogenesis by suppressing NF-κB activation through blockade of p65 nuclear translocation. These results provide a solid preclinical foundation for combining β-lapachone with TMZ as a promising strategy to counteract TMZ resistance in GBM.</p>

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β-Lapachone sensitizes glioblastoma to Temozolomide by inhibiting NF-κB signaling

  • 期刊论文

  • 发表日期：

    2025年12月3日

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  • Chunhua Quan,
  • Ying Liu,
  • Yuan Gao,
  • Houkun Zhou,
  • Haiyan Quan,
  • Anna Han,
  • Xiaodan Lu,
  • Zhenhua Lin

摘要

Temozolomide (TMZ) constitutes the first-line chemotherapeutic regimen for glioblastoma (GBM), yet its clinical efficacy remains suboptimal. β-lapachone, a naturally occurring NQO1 inhibitor, has demonstrated potent antitumor activity across multiple malignancies. Based on the critical involvement of nuclear factor-κB (NF-κB) in GBM pathogenesis, this study investigated whether β-lapachone can enhance the antitumor effect of TMZ by targeting the NF-κB pathway using both in vitro and in vivo models. We found that β-lapachone acts synergistically with TMZ to inhibit GBM cell proliferation, epithelial–mesenchymal transition (EMT), and angiogenesis by suppressing NF-κB activation through blockade of p65 nuclear translocation. These results provide a solid preclinical foundation for combining β-lapachone with TMZ as a promising strategy to counteract TMZ resistance in GBM.