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  1. Home
  3. Michelia Compressa-derived Santamarine Inhibits Oral Cancer Cell Proliferation Via Oxidative Stress-mediated Apoptosis And Dna Damage.
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  3. Michelia Compressa-derived Santamarine Inhibits Oral Cancer Cell Proliferation Via Oxidative Stress-mediated Apoptosis And Dna Damage.

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Michelia compressa-Derived Santamarine Inhibits Oral Cancer Cell Proliferation via Oxidative Stress-Mediated

Hsin-I Lu1, Kuan-Liang Chen2, Ching-Yu Yen2,3

  • 1Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 80708, Taiwan.

Pharmaceuticals (Basel, Switzerland)
|February 24, 2024

View abstract on PubMed

Summary
This summary is machine-generated.

Santamarine (SAMA) selectively targets oral cancer cells by inducing oxidative stress and DNA damage, leading to apoptosis. This natural compound shows promise for oral cancer treatment with minimal impact on normal cells.

Keywords:
apoptosisevergreen treenatural productoral canceroxidative stress

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Area of Science:

  • Natural Product Chemistry
  • Cancer Biology
  • Oxidative Stress Research

Background:

  • The therapeutic potential of santamarine (SAMA), a natural product from Michelia compressa var. compressa, against oral cancer is largely unknown.
  • Understanding the selective mechanisms of SAMA against oral cancer cells is crucial for developing novel treatments.

Purpose of the Study:

  • To investigate the anticancer effects of SAMA on oral cancer cell lines (OC-2 and HSC-3).
  • To elucidate the underlying mechanisms of SAMA's action, focusing on oxidative stress and apoptosis.
  • To evaluate the selectivity of SAMA towards cancer cells compared to normal cells.

Main Methods:

  • Cell viability assays were performed on oral cancer and normal cells treated with SAMA.
  • Oxidative stress markers, including reactive oxygen species (ROS), mitochondrial superoxide, and glutathione levels, were measured.
  • Cell cycle progression was analyzed using flow cytometry.
  • Apoptosis was assessed via Annexin V staining and caspase activation assays.
  • DNA damage markers (γH2AX, 8-hydroxy-2-deoxyguanosine) were evaluated.
  • The role of oxidative stress was confirmed using N-acetylcysteine (NAC).

    • Main Results:

    • SAMA selectively inhibited the viability of oral cancer cells more than normal cells.
    • SAMA induced significant oxidative stress in cancer cells, evidenced by increased ROS and mitochondrial superoxide, and depleted glutathione.
    • SAMA treatment led to G2/M cell cycle arrest and triggered apoptosis in oral cancer cells.
    • SAMA enhanced DNA damage in oral cancer cells.
    • These effects were attenuated by NAC, confirming the ROS-dependent mechanism.
    • The observed anticancer effects were concentration- and time-dependent and more pronounced in cancer cells.

    Conclusions:

    • SAMA exhibits selective antiproliferative effects against oral cancer cells through a mechanism dependent on induced oxidative stress.
    • SAMA triggers apoptosis and DNA damage in oral cancer cells while minimizing cytotoxicity to normal cells.
    • SAMA represents a potential therapeutic agent for oral cancer, warranting further investigation.