2. Academic Validation
  3. The Study of the Antitumor Effects and Molecular Mechanisms of Byakangelicol on HepG2 Cells

The Study of the Antitumor Effects and Molecular Mechanisms of Byakangelicol on HepG2 Cells

  • J Biochem Mol Toxicol. 2026 Apr;40(4):e70819. doi: 10.1002/jbt.70819.
Chang Wang 1 2,  Xiao-Yu Jin 3,  Ying-Hua Luo 4,  Nan Wu 1 5 6,  Yan-Jun Tang 1 6,  Yan-Zhi Liu 1 5 6,  Tian-Zhu Li 7,  Cheng-Hao Jin 1 5 6
Affiliations

Affiliations

  • 1 Department of Food Science and Engineering, College of Food Science, Heilongjiang Bayi Agricultural University, Daqing, China.
  • 2 Agricultural Products and Proceed Products Supervision and Testing Center, Ministry of Agriculture, Daqing, China.
  • 3 Department of CT, Daqing Oilfield General Hospital, Daqing, China.
  • 4 Department of Grass Science, College of Animal Science and Veterinary Medicine, Heilongjiang Bayi Agricultural University, Daqing, China.
  • 5 Department of Biochemistry and Molecular Biology, College of Life Science and Technology, Heilongjiang Bayi Agricultural University, Daqing, China.
  • 6 National Coarse Cereals Engineering Research Center, Daqing, China.
  • 7 Department of Molecular Biology, College of Basic Medical Science, Chifeng University, Inner Mongolia Autonomous Region, Chifeng, China.
PMID: 41891544 DOI: 10.1002/jbt.70819
Abstract

Byakangelicol (BYA) belongs to Coumarins, which have anti-inflammatory and anti-tumor pharmacological properties, but its inhibitory effect on liver Cancer and its mechanism are still indistinct. This study explored the mechanism of action by which BYA affects hepatocellular carcinoma (HCC). Cell cytotoxic and Apoptosis assay results showed that BYA effectively killed three kinds of HCC cells and induced mitochondrial pathway Apoptosis of HepG2 cells. Furthermore, the results of network pharmacological analysis, flow cytometry and western blot assays demonstrated that BYA can induced Reactive Oxygen Species (ROS) accumulation, which in turn upregulated the phosphorylation expression of JNK and p38 while downregulating the phosphorylation expression of Akt, ERK, and STAT3. Meanwhile, the expression of these proteins was reversed after MAPK inhibitors pretreatment. Cell cycle and cell metastasis assay results showed that BYA can induce G2/M phase arrest and inhibit cell metastasis. At the same time, the expression of related proteins was reversed after ROS inhibitors (N-Acetyl-l-cysteine) pretreatment. The research results reveal that BYA can cause the accumulation of ROS within cells, and induce Apoptosis in HepG2 cells through the mitochondrial pathway, thereby leading to cell cycle arrest at the G2/M phase and inhibition of cell migration ability. This study provides theoretical support for the clinical application of BYA in the treatment of HCC.

Keywords

ROS; byakangelicol; cell apoptosis; cell cycle; cell migration; hepatocellular carcinoma.

Figures
Products