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Background <p>3-Hydroxy-1-(3’,5’-dimethoxy-4’-hydroxy-phenyl)-hexan-5-one (3-HDM), a novel ginger <i>Zingiber officinale</i>-derived compound, lacks anti-cancer investigation, especially for oral cancer. This study addresses the antioral function and mechanism of 3-HDM against oral cancer cells (Ca9-22 and CAL 27).</p> Method <p>MTS, flow cytometry, and western blotting were used to determine cell viability and antioral function and mechanism.</p> Results <p>3-HDM inhibits oral cancer cell viability without normal cell (S-G) toxicity. This selective antiproliferation relies on oxidative stress validated by <i>N</i>-acetylcysteine (NAC), a reactive oxygen species (ROS) remover. 3-HDM upregulates subG1 and annexin V proportions, enhances caspases 3 and 8 activation to a greater extent in oral cancer than in normal cells, reverted by NAC. This process demonstrates the ROS-dependent selective apoptotic character of 3-HDM. 3-HDM also upregulates more ROS and mitochondrial superoxide and downregulates the mitochondrial membrane potential and glutathione in oral cancer than in normal cells in a ROS-dependent manner. Moreover, 3-HDM suppresses antioxidant signaling mRNA expressions such as <i>NFE2L2</i>, <i>NQO1</i>, and <i>TXN</i> and inhibits NFE2L2 phosphorylation in oral cancer cells compared to normal cells. NAC also downregulates the 3-HDM-induced γH2AX and 8-hydroxy-2-deoxyguanosine DNA damage markers.</p> Conclusion <p>3-HDM shows selective antioral cancer effects and mechanisms without toxicity to normal cells via oxidative stress regulation.</p>

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Antioral cancer effects of ginger derivative 3-HDM exert oxidative stress-associated apoptosis and DNA damage

  • 期刊论文

  • 发表日期：

    2025年4月23日

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  • Kuan-Liang Chen,
  • Hsin-I Lu,
  • Ching-Yu Yen,
  • Chung-Yi Chen,
  • Tsu-Ming Chien,
  • Jiiang-Huei Jeng,
  • Bing-Hung Chen,
  • Hsueh-Wei Chang

摘要

Background

3-Hydroxy-1-(3’,5’-dimethoxy-4’-hydroxy-phenyl)-hexan-5-one (3-HDM), a novel ginger Zingiber officinale-derived compound, lacks anti-cancer investigation, especially for oral cancer. This study addresses the antioral function and mechanism of 3-HDM against oral cancer cells (Ca9-22 and CAL 27).

Method

MTS, flow cytometry, and western blotting were used to determine cell viability and antioral function and mechanism.

Results

3-HDM inhibits oral cancer cell viability without normal cell (S-G) toxicity. This selective antiproliferation relies on oxidative stress validated by N-acetylcysteine (NAC), a reactive oxygen species (ROS) remover. 3-HDM upregulates subG1 and annexin V proportions, enhances caspases 3 and 8 activation to a greater extent in oral cancer than in normal cells, reverted by NAC. This process demonstrates the ROS-dependent selective apoptotic character of 3-HDM. 3-HDM also upregulates more ROS and mitochondrial superoxide and downregulates the mitochondrial membrane potential and glutathione in oral cancer than in normal cells in a ROS-dependent manner. Moreover, 3-HDM suppresses antioxidant signaling mRNA expressions such as NFE2L2, NQO1, and TXN and inhibits NFE2L2 phosphorylation in oral cancer cells compared to normal cells. NAC also downregulates the 3-HDM-induced γH2AX and 8-hydroxy-2-deoxyguanosine DNA damage markers.

Conclusion

3-HDM shows selective antioral cancer effects and mechanisms without toxicity to normal cells via oxidative stress regulation.