Galangin potentiates human breast cancer to apoptosis induced by TRAIL through activating AMPK

Wei Song1, Chong-Yang Yan2, Qian-Qian Zhou3

  • 1Huai'an First People's Hospital, Nanjing Medical University,No.6 Beijing West Road, Huaiyin District, Huai'an, Jiangsu, 223001, China.

Insights

Galangin enhances TRAIL-induced apoptosis in breast cancer by activating the AMPK signaling pathway. This natural compound sensitizes cancer cells to TRAIL, promoting cell death via Caspase-3 activation.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Breast cancer is a leading cause of cancer death in women, with limited treatment options.
  • Galangin, a natural flavonoid, shows potential anti-cancer properties.
  • Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a promising anti-cancer agent for breast cancer.

Purpose of the Study:

  • To investigate the mechanism by which galangin enhances TRAIL-induced apoptosis in human breast cancer cells.
  • To explore the role of endoplasmic reticulum (ER) stress and the adenosine monophosphate-activated protein kinase (AMPK) signaling pathway in galangin's anti-cancer effects.

Main Methods:

  • Human breast cancer cell lines were treated with galangin and/or TRAIL.
  • Expression levels of CHOP, DR4, and activated Caspase-3 were analyzed.
  • AMPK phosphorylation was assessed.
  • The effects of AMPK inhibition and silencing on cell apoptosis were evaluated.

Main Results:

  • Galangin upregulated CHOP and DR4 expression, sensitizing cells to TRAIL-induced apoptosis.
  • Galangin-induced apoptosis was mediated by Caspase-3 activation and associated with AMPK phosphorylation.
  • Inhibition or silencing of AMPK diminished the combined anti-cancer effects of galangin and TRAIL.

Conclusions:

  • Galangin effectively promotes TRAIL-induced apoptosis in human breast cancer cells via the TRAIL/Caspase-3/AMPK signaling pathway.
  • Activating the AMPK pathway with galangin may enhance TRAIL-based anti-cancer therapeutic strategies.

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