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The Chemopreventive Effect of Ginsenoside Compound K Is Regulated by PARP-1 Hyperactivation, Which Is Promoted by

Sang-Hun Kim1, Sung-Hwan Ki2, Seok-Woo Hyeong3

  • 1Department of Anesthesiology and Pain Medicine, School of Medicine, Chosun University, 309 Pilmundaero, Dong-gu, Gwangju 61452, Republic of Korea.

Nutrients
|February 13, 2025
PubMed
Abstract

Insights

Ginsenoside compound K (CK) triggers cancer cell death via PARP-1 activation and SIRT6 degradation in lung cancer. This study reveals CK’s anticancer mechanism, highlighting SIRT6 as a potential biomarker for its chemopreventive effects.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Ginsenoside compound K (CK), a ginseng metabolite, shows anticancer potential.
  • The precise molecular mechanisms of CK's action in lung cancer are not fully understood.
  • Investigating the roles of silent information regulator 6 (SIRT6) and poly (ADP-ribose) polymerase 1 (PARP-1) in CK's effects is crucial.

Purpose of the Study:

  • To elucidate the molecular mechanisms underlying the anticancer effects of ginsenoside compound K (CK) in lung cancer.
  • To investigate the involvement of silent information regulator 6 (SIRT6) and poly (ADP-ribose) polymerase 1 (PARP-1) in CK-induced lung cancer cell death.
  • To determine if SIRT6 can serve as a biomarker for CK's chemopreventive efficacy.

Main Methods:

  • Cell proliferation assays were performed on H460 lung cancer cells treated with CK.
  • Western blotting, immunofluorescence, and immunoprecipitation were used to analyze protein levels and interactions.
  • Levels of SIRT6, PARP-1, p62, and apoptosis markers were assessed.
  • Autophagy markers (LC3-II) and DNA damage markers (gamma-H2AX) were evaluated.

Main Results:

  • CK induced PARP-1 activation and parthanatos, a form of programmed cell death, through SIRT6 degradation mediated by sequestosome-1/p62.
  • CK inhibited H460 cell proliferation and upregulated DNA damage and cell cycle arrest markers (p27, p21, phospho-p53, gamma-H2AX).
  • PARP-1 activation was inversely correlated with SIRT6 levels, suggesting complementary roles in CK's anti-proliferative effects.

Conclusions:

  • PARP-1 activation, promoted by p62-mediated SIRT6 degradation, is a key mechanism in CK-induced growth inhibition of lung cancer cells.
  • SIRT6 degradation plays a critical role in CK's anticancer activity.
  • SIRT6 emerges as a potential biomarker for the chemopreventive effects of CK in lung cancer, warranting further clinical investigation.
Keywords:
PARP-1 protein activationSIRT6 proteinginsenoside compound Klung cancerp62 protein

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