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Notoginsenoside R1 induces DNA damage via PHF6 protein to inhibit cervical carcinoma cell proliferation

Ting Cai1, Wenquan Wu2, Longhua Guo2

  • 1Department of Acupuncture and Moxibustion, Shenzhen Second People's Hospital, The First Affiliated Hospital of Shenzhen University, Shenzhen, Guangdong 518055, P.R. China.

Molecular Medicine Reports
|February 4, 2021
PubMed

Insights

Notoginsenoside R1 (NGR1) inhibits cervical cancer cell growth by inducing DNA damage and apoptosis. This traditional medicine compound may serve as a novel chemotherapeutic agent for cervical carcinoma.

Area of Science:

  • Pharmacology
  • Oncology
  • Molecular Biology

Background:

  • Notoginsenoside R1 (NGR1), a component of traditional Chinese medicine, shows potential in inhibiting cancer cell proliferation.
  • The precise mechanisms by which NGR1 affects cervical carcinoma remain largely unelucidated.

Purpose of the Study:

  • To investigate the antitumor effects of NGR1 on cervical carcinoma cell lines (CaSki and HeLa) in vitro.
  • To elucidate the molecular mechanisms underlying NGR1's action on cervical cancer cells.

Main Methods:

  • Cell viability assays (Cell Counting Kit-8) and colony formation assays were performed.
  • Apoptosis, cell cycle progression, and protein expression (cyclins, CDKs, DNA damage markers) were analyzed using DAPI staining, flow cytometry, and western blotting.

Main Results:

  • NGR1 significantly suppressed the viability and colony formation of cervical cancer cells.
  • NGR1 induced apoptosis, S-phase cell cycle arrest, and altered expression of cyclins (upregulating cyclin A2 and CDK2, downregulating cyclin D1).
  • NGR1 triggered DNA damage response by phosphorylating H2AX and ATR, downregulating PHF6, and upregulating p53.

Conclusions:

  • NGR1 inhibits cervical carcinoma cell viability and induces apoptosis, potentially through DNA damage pathways activated by PHF6 downregulation and H2AX/ATR phosphorylation.
  • NGR1 also causes S-phase arrest and affects cyclin/CDK expression, suggesting its potential as a novel chemotherapeutic agent for cervical cancer.
Keywords:
DNA damagecell proliferationapoptosisplant homeodomain finger protein 6

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