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<p>Calanthe arisanensis, a traditional medicinal orchid, contains Calanquinone A, a quinone-type compound with reported anticancer properties. Glioblastoma multiforme (GBM) is a highly aggressive brain tumor with limited treatment options and a poor prognosis. This study investigates the molecular mechanisms underlying the antiproliferative and antimigratory effects of Calanquinone A in GBM. Human GBM cell lines (U87MG) and patient-derived primary GBM cells (Pt#3) were treated with Calanquinone A (1–2.5 µM), and effects on cell viability, proliferation, and migration were assessed using CCK-8, trypan blue exclusion, colony formation, wound healing, transwell migration, and F-actin staining assays. Calanquinone A significantly reduced GBM cell viability and migration. Western blot analysis revealed that Calanquinone A inhibited STAT3 phosphorylation at Tyr705, leading to downregulation of its downstream targets c-Myc and MMP9. STAT3 overexpression reversed these effects, confirming the involvement of STAT3-dependent pathways. In a mouse xenograft model, Calanquinone A suppressed tumor formation in vivo. Molecular docking analysis further revealed a potential direct interaction between Calanquinone A and STAT3, supporting a direct mechanism of action. These findings demonstrate that Calanquinone A exerts potent antitumor effects in glioblastoma by targeting the STAT3/c-Myc and STAT3/MMP9 signaling axes, supporting its potential as a natural STAT3-targeting agent for GBM therapy.</p> Graphical abstract <p></p>

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Calanquinone A suppresses glioma progression via STAT3-mediated regulation of c-Myc and MMP9

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年8月4日

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  • Wen-Chi Hsieh,
  • Chun-Yu Lin,
  • Hsuan‐Cheng Wu,
  • Huang-Wei Lo,
  • Chiung-Yuan Ko,
  • Jian-Ying Chuang,
  • Tsung-I. Hsu,
  • Tsui-Hwa Tseng,
  • Teng-Wei Huang,
  • Shao-Ming Wang

摘要

Calanthe arisanensis, a traditional medicinal orchid, contains Calanquinone A, a quinone-type compound with reported anticancer properties. Glioblastoma multiforme (GBM) is a highly aggressive brain tumor with limited treatment options and a poor prognosis. This study investigates the molecular mechanisms underlying the antiproliferative and antimigratory effects of Calanquinone A in GBM. Human GBM cell lines (U87MG) and patient-derived primary GBM cells (Pt#3) were treated with Calanquinone A (1–2.5 µM), and effects on cell viability, proliferation, and migration were assessed using CCK-8, trypan blue exclusion, colony formation, wound healing, transwell migration, and F-actin staining assays. Calanquinone A significantly reduced GBM cell viability and migration. Western blot analysis revealed that Calanquinone A inhibited STAT3 phosphorylation at Tyr705, leading to downregulation of its downstream targets c-Myc and MMP9. STAT3 overexpression reversed these effects, confirming the involvement of STAT3-dependent pathways. In a mouse xenograft model, Calanquinone A suppressed tumor formation in vivo. Molecular docking analysis further revealed a potential direct interaction between Calanquinone A and STAT3, supporting a direct mechanism of action. These findings demonstrate that Calanquinone A exerts potent antitumor effects in glioblastoma by targeting the STAT3/c-Myc and STAT3/MMP9 signaling axes, supporting its potential as a natural STAT3-targeting agent for GBM therapy.

Graphical abstract