ArticleMolecular biology reports2025
Antioral cancer effects of ginger derivative 3-HDM exert oxidative stress-associated apoptosis and DNA damage.
Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
background3-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).
methodMTS, flow cytometry, and western blotting were used to determine cell viability and antioral function and mechanism.
results3-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.
conclusion3-HDM shows selective antioral cancer effects and mechanisms without toxicity to normal cells via oxidative stress regulation.
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