Scholarlink

<p>Glioma is a highly aggressive brain tumor with limited treatment options. Natural compounds offer promising therapeutic alternatives due to their safety and low toxicity. Morusinol, a flavonoid from Morus alba, exhibits anti-tumor effects in various cancers, but its role in glioma remains unknown. This study demonstrates that Morusinol significantly inhibits proliferation, migration, invasion, and colony formation of LN229 and U251 glioma cells, with IC50 values around 20&#xa0;μM. It induces apoptosis by increasing ROS levels and modulating Bcl-2 family proteins and caspase-3 activation. Network pharmacology and molecular docking predict strong binding of Morusinol to key PI3K/AKT pathway components, including p110α, p85α, PDK1, and PTEN. Western blotting confirms that Morusinol suppresses AKT and mTOR phosphorylation, indicating pathway inhibition. Importantly, co-treatment with UCL-TRO-1938, a p110α activator, partially reverses Morusinol-induced suppression of AKT phosphorylation and cell proliferation, supporting target specificity. These results indicate that Morusinol exerts potent anti-glioma effects primarily through inhibition of the PI3K/AKT/mTOR signaling pathway. Our findings highlight Morusinol as a promising natural agent for glioma therapy.</p> Graphical abstract <p></p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Morusinol exerts anti-glioma activity by targeting the PI3K/AKT/mTOR signaling pathway

  • 期刊论文

  • 发表日期：

    2026年2月10日

查看全文
  • Zhiyong Jin,
  • Changzhou Xiao,
  • Sicheng Ma,
  • Gang Li,
  • Mengyao Zhu,
  • Feifan Zhang,
  • Hanyu Zhang,
  • Rutong Yu

摘要

Glioma is a highly aggressive brain tumor with limited treatment options. Natural compounds offer promising therapeutic alternatives due to their safety and low toxicity. Morusinol, a flavonoid from Morus alba, exhibits anti-tumor effects in various cancers, but its role in glioma remains unknown. This study demonstrates that Morusinol significantly inhibits proliferation, migration, invasion, and colony formation of LN229 and U251 glioma cells, with IC50 values around 20 μM. It induces apoptosis by increasing ROS levels and modulating Bcl-2 family proteins and caspase-3 activation. Network pharmacology and molecular docking predict strong binding of Morusinol to key PI3K/AKT pathway components, including p110α, p85α, PDK1, and PTEN. Western blotting confirms that Morusinol suppresses AKT and mTOR phosphorylation, indicating pathway inhibition. Importantly, co-treatment with UCL-TRO-1938, a p110α activator, partially reverses Morusinol-induced suppression of AKT phosphorylation and cell proliferation, supporting target specificity. These results indicate that Morusinol exerts potent anti-glioma effects primarily through inhibition of the PI3K/AKT/mTOR signaling pathway. Our findings highlight Morusinol as a promising natural agent for glioma therapy.

Graphical abstract