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Ginsenoside Rg3 regulates DNA damage in non-small cell lung cancer cells by activating VRK1/P53BP1 pathway

Tianhua Liu1, Ling Zuo1, Dongqing Guo2

  • 1School of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing, China.

Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie
|October 20, 2019
PubMed

Insights

Ginsenoside Rg3 protects lung cancer cells from DNA damage and inhibits tumor growth by upregulating VRK1 expression and P53BP1 foci formation. This reveals new therapeutic targets for lung cancer prevention and treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Lung cancer is a leading cause of cancer-related mortality.
  • Ginsenoside Rg3, derived from Ginseng, shows promise in treating non-small cell lung cancer (NSCLC).
  • Previous research indicates Rg3 may induce DNA damage to combat NSCLC, but its anti-DNA damaging effects and mechanisms require further elucidation.

Purpose of the Study:

  • To investigate the effects of Ginsenoside Rg3 on DNA repair mechanisms in lung cancer.
  • To explore the role of the VRK1/P53BP1 signaling pathway in Ginsenoside Rg3's anti-cancer activity.
  • To understand the anti-tumorigenic mechanisms of Ginsenoside Rg3 in NSCLC.

Main Methods:

  • Utilized a mouse model of urethane-induced lung cancer.
  • Performed cell survival assays and single-cell gel electrophoresis to assess DNA damage and cell viability.
  • Quantified VRK1 mRNA and protein expression using RT-qPCR and Western blot.
  • Employed immunofluorescence assays to observe VRK1 and P53BP1 protein localization.
  • Conducted experiments with VRK1-knockdown cells for validation.

Main Results:

  • Ginsenoside Rg3 treatment reduced lung cancer incidence and invasion in vivo.
  • Rg3 protected lung adenocarcinoma cells from DNA damage and inhibited proliferation in vitro.
  • Rg3 significantly increased VRK1 mRNA and protein expression in NSCLC cells.
  • Observed increased P53BP1 foci formation and VRK1 nuclear-cytoplasmic translocation.
  • VRK1 knockdown reversed the protective effects of Rg3, confirming its role.

Conclusions:

  • Ginsenoside Rg3 upregulates VRK1 expression and promotes P53BP1 foci formation in response to DNA damage.
  • These actions inhibit lung cancer cell tumorigenesis and viability.
  • Rg3's mechanism involves regulating the VRK1/P53BP1 pathway, offering potential therapeutic targets for lung cancer.
Keywords:
Ginsenoside Rg3NSCLCP53BP1TCMVRK1

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