ArticleMolecular biology reports2025
Ginger-derived 1-(4'-hydroxy-3'-methoxyphenyl)-5-methoxydecan-3-one (HMPM) induces apoptosis and DNA damage against triple-negative breast cancer cells in vitro.
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
backgroundGinger contains many biocompounds, but the antiproliferative effects of its phenylalkanoids (such as 1-(4'-hydroxy-3'-methoxyphenyl)-5-methoxydecan-3-one (HMPM)) on cancer cells are rarely reported. This study aims to explore the antiproliferative effects and mechanisms of HMPM on triple-negative breast cancer (TNBC) cells.
methodsATP-based viability, flow cytometry, and Western blotting were conducted to explore the anti-TNBC in vitro effects and mechanisms.
resultsHMPM inhibits the proliferation of several breast cancer cell lines. Two TNBC cell lines (Hs578T and MDA-MB-231), showing the highest sensitivity to HMPM, exhibited oxidative stress-dependent antiproliferation, as validated by N-acetylcysteine (NAC). Regarding flow cytometry, HMPM changes cell cycle distribution; upregulates apoptosis (annexin V), reactive oxygen species, and mitochondrial oxidative stress; and downregulates mitochondrial membrane potential and glutathione to a greater extent in TNBC cells than in normal breast cells (H184B5F5/M10), attenuated by NAC. Regarding flow cytometry and Western blotting, HMPM notably triggers oxidative stress-mediated caspase 3 and 8 activation in TNBC cells compared to M10 cells. Finally, HMPM causes oxidative DNA damage, as indicated by γH2AX and 8-hydroxy-2-deoxyguanosine flow cytometry.
conclusionTaken together, the ginger-derived HMPM offers antiproliferative activity against TNBC cells via oxidative stress-dependent changes with limited cytotoxicity to normal cells.
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