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Licochalcone B Ameliorates Liver Cancer via Targeting of Apoptotic Genes, DNA Repair Systems, and Cell Cycle Control

Kadry Sadek1, Tarek Abouzed2, Sherif Nasr3

  • 1Department of Biochemistry, Faculty of Veterinary Medicine, Damanhur University, Egypt.

Iranian Journal of Pharmaceutical Research : IJPR
|April 12, 2021
PubMed

Insights

Licochalcone B and fullerene C60 nanoparticles show promise in combating liver cancer by reducing DNA damage and promoting apoptosis. These compounds target key proteins involved in DNA repair and cell cycle regulation, offering a potential new therapeutic strategy.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cancer Research

Background:

  • Apurinic/apyrimidinic endonuclease 1/redox factor-1 (APE1/Ref-1) is crucial for DNA repair and transcription factor regulation.
  • Cyclin-dependent kinases (CDKs) control cell-cycle progression.
  • Hepatocarcinoma is a significant health concern with complex underlying molecular mechanisms.

Purpose of the Study:

  • To evaluate the synergistic anti-cancer effects of licochalcone B (LCB) and fullerene C60 (FnC60) nanoparticles on diethylnitrosamine (DEN)-induced hepatocarcinoma in rats.
  • To investigate the impact of LCB and FnC60 on key molecular pathways, including DNA repair (APE1/Ref-1) and cell-cycle control (CDK-4).

Main Methods:

  • Induction of hepatocarcinoma in rats using diethylnitrosamine (DEN).
  • Treatment with licochalcone B (LCB) alone and in combination with fullerene C60 (FnC60) nanoparticles.
  • Assessment of DNA fragmentation, oxidative DNA damage (8-hydroxy-2'-deoxyguanosine), and mRNA/protein expression of key genes (APE1/Ref-1, CDK-4, p53, Bax, Bcl-2, Bcl-xL, β-arrestin-2) and proteins.

Main Results:

  • LCB and FnC60 significantly reduced DNA fragmentation and oxidative DNA damage.
  • Combined treatment decreased the expression of APE1/Ref-1, CDK-4, retinoblastoma, Bcl-2, Bcl-xL, and β-arrestin-2.
  • LCB and FnC60 increased the expression of p53, Bax, and caspase-3, indicating apoptosis induction.
  • FnC60 potentiated the therapeutic effects of LCB at the molecular level.

Conclusions:

  • LCB, alone or with FnC60, demonstrates significant protective effects against DEN-induced hepatocarcinogenesis in rats.
  • The observed effects are attributed to the regulation of DNA repair enzymes and cell-cycle control proteins, alongside the induction of apoptosis.
  • FnC60 enhances LCB's efficacy, potentially by targeting cancer cells, suggesting a promising synergistic therapeutic approach for liver cancer.
Keywords:
ApoptosisDNA repair systemLicochalcone BLiver cancerSignaling pathways

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