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<p>Monotropein (Mon) is an iridoid glycosides extracted from <i>Morinda</i> <i>officinalis</i> F.C. How. (Rubiaceae) that shows anticancer effects on colorectal cancer. This study aimed to investigate the therapeutic effect of Mon on lung cancer. The viability, apoptosis, invasion, and tube formation of A549 and H1299 were determined by CCK8 assay, flow cytometry, transwell assay, and tube formation assay. NF-κB expression in the nucleus was detected by immunofluorescent staining. In vivo assay, BALB/c nude mice were divided into a sham group and a 2&#xa0;mg/kg Mon group. For the Mon group, mice were orally administered with 2&#xa0;mg/kg Mon. The duration of the animal study was 35&#xa0;days, and the tumor formation and angiogenesis were investigated. Compared with the control (Mon 0&#xa0;μM) group, Mon dramatically repressed the viability, invasion, tube formation, proliferation marker Ki67, N-cadherin, and VEGFA expressions in A549 cells (Mon of 25, 50, and 100&#xa0;µM) and H1299 cells (Mon of 50 and 100&#xa0;µM). Mon dramatically promoted cell apoptosis, cleaved caspase 3, and E-cadherin expressions. Besides, Mon remarkably downregulated p-AKT and p-NF-κB protein expressions. Moreover, AKT agonist SC79 reversed the anticancer effects of 100&#xa0;µM Mon on A549 cells. Furthermore, Mon markedly suppressed tumor growth, decreased N-cadherin, VEGFA, p-AKT, and p-NF-κB expressions, increased apoptosis and E-cadherin expression, and SC79 reversed the inhibition effects of Mon in vivo. Thus, Mon is a potential antitumor natural drug, and more signaling pathways involved in Mon-modulated lung cancer progression are worth testing for further investigation.</p> Graphical abstract <p></p>

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Monotropein represses the proliferation and angiogenesis via the AKT/NF-κB pathway in lung cancer

  • 期刊论文

  • 发表日期：

    2025年1月29日

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  • Bao-ning Cai,
  • Bo Ma,
  • Sheng Zhang,
  • Wei He

摘要

Monotropein (Mon) is an iridoid glycosides extracted from Morinda officinalis F.C. How. (Rubiaceae) that shows anticancer effects on colorectal cancer. This study aimed to investigate the therapeutic effect of Mon on lung cancer. The viability, apoptosis, invasion, and tube formation of A549 and H1299 were determined by CCK8 assay, flow cytometry, transwell assay, and tube formation assay. NF-κB expression in the nucleus was detected by immunofluorescent staining. In vivo assay, BALB/c nude mice were divided into a sham group and a 2 mg/kg Mon group. For the Mon group, mice were orally administered with 2 mg/kg Mon. The duration of the animal study was 35 days, and the tumor formation and angiogenesis were investigated. Compared with the control (Mon 0 μM) group, Mon dramatically repressed the viability, invasion, tube formation, proliferation marker Ki67, N-cadherin, and VEGFA expressions in A549 cells (Mon of 25, 50, and 100 µM) and H1299 cells (Mon of 50 and 100 µM). Mon dramatically promoted cell apoptosis, cleaved caspase 3, and E-cadherin expressions. Besides, Mon remarkably downregulated p-AKT and p-NF-κB protein expressions. Moreover, AKT agonist SC79 reversed the anticancer effects of 100 µM Mon on A549 cells. Furthermore, Mon markedly suppressed tumor growth, decreased N-cadherin, VEGFA, p-AKT, and p-NF-κB expressions, increased apoptosis and E-cadherin expression, and SC79 reversed the inhibition effects of Mon in vivo. Thus, Mon is a potential antitumor natural drug, and more signaling pathways involved in Mon-modulated lung cancer progression are worth testing for further investigation.

Graphical abstract