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Background <p>Ginger 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.</p> Methods <p>ATP-based viability, flow cytometry, and Western blotting were conducted to explore the anti-TNBC in vitro effects and mechanisms.</p> Results <p>HMPM 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 <i>N</i>-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.</p> Conclusion <p>Taken together, the ginger-derived HMPM offers antiproliferative activity against TNBC cells via oxidative stress-dependent changes with limited cytotoxicity to normal cells.</p>

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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

  • 期刊论文

  • 发表日期：

    2025年10月16日

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  • Min-Yu Lee,
  • Wan-Ling Tseng,
  • Zong-Ying Yang,
  • Tsu-Ming Chien,
  • Chien-Chih Chiu,
  • Yi-Hao Lo,
  • Chung-Yi Chen,
  • Hsueh-Wei Chang

摘要

Background

Ginger 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.

Methods

ATP-based viability, flow cytometry, and Western blotting were conducted to explore the anti-TNBC in vitro effects and mechanisms.

Results

HMPM 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.

Conclusion

Taken together, the ginger-derived HMPM offers antiproliferative activity against TNBC cells via oxidative stress-dependent changes with limited cytotoxicity to normal cells.