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Subamolide a induces mitotic catastrophe accompanied by apoptosis in human lung cancer cells

Jen-Yu Hung1, Ching-Wen Wen, Ya-Ling Hsu

  • 1Division of Pulmonary and Critical Care Medicine, Kaohsiung Medical University Hospital, Kaohsiung 807, Taiwan ; Department of Internal Medicine, Kaohsiung Municipal Ta-Tung Hospital, Kaohsiung 801, Taiwan.

Evidence-Based Complementary and Alternative Medicine : Ecam
|March 28, 2013
PubMed

Insights

Subamolide A, a compound from Cinnamomum subavenium, effectively reduced non-small cell lung cancer cell viability and tumor size. It induces cancer cell death through oxidant stress, mitotic catastrophe, and apoptosis, suggesting its potential as a novel anticancer agent.

Area of Science:

  • Pharmacology
  • Molecular Biology
  • Oncology

Background:

  • Non-small cell lung cancer (NSCLC) remains a leading cause of cancer-related mortality.
  • Novel therapeutic agents are urgently needed to improve treatment outcomes for NSCLC.
  • Cinnamomum subavenium is a plant with traditional medicinal uses.

Purpose of the Study:

  • To investigate the anticancer effects of subamolide A (Sub-A) on human non-small cell lung cancer cell lines.
  • To elucidate the molecular mechanisms underlying Sub-A-induced cancer cell death.
  • To evaluate the efficacy of Sub-A in an in vivo animal model.

Main Methods:

  • Cell viability assays on A549 and NCI-H460 cell lines treated with Sub-A.
  • Analysis of reactive oxygen species (ROS) production and glutathione levels.
  • Investigation of the role of ATM, ATF3, and p53 signaling pathways.
  • Assessment of mitotic catastrophe and apoptosis induction.
  • Tumor xenograft model in animals to evaluate in vivo efficacy.

Main Results:

  • Sub-A significantly decreased cell viability in both A549 and NCI-H460 lung cancer cells.
  • Sub-A induced cancer cell death via mitotic catastrophe and apoptosis, mediated by ROS generation.
  • Elevated ROS activated ATM, leading to ATF3 upregulation and enhanced p53 phosphorylation.
  • An antioxidant (EUK8) and shRNA targeting ATM/ATF3 attenuated Sub-A's effects.
  • Sub-A treatment resulted in a 70% reduction in tumor size in an animal model.

Conclusions:

  • Sub-A exhibits potent anticancer activity against non-small cell lung cancer.
  • The mechanism involves ROS-mediated activation of ATM/ATF3/p53 signaling, leading to mitotic catastrophe and apoptosis.
  • Sub-A demonstrates significant in vivo efficacy, supporting its potential as a novel therapeutic agent for NSCLC.

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