Arctigenin induces apoptosis in human hepatoblastoma cells

Atsuki Naoe, Tomonori Tsuchiya, Yasuhiro Kondo, Naoko Uga, Shunsuke Watanabe, Toshihiro Yasui, Fujio Hara, Tatsuya Suzuki

Research output: Contribution to journalArticlepeer-review

9 Citations (Scopus)


Purpose: Arctigenin has been shown to have anti-tumor effects in various types of cancers. This study was conducted to verify these effects in the human-derived hepatoblastoma cell line, HUH-6 clone 5 (hereinafter, HUH-6). Methods: Arctigenin was added to cultured HUH-6 cells, and cellular activity was evaluated by MTS assay. To determine the relationship between reduced cellular activity and apoptosis, we measured the activities of caspase 3/7, 8, and 9 and conducted flow cytometry with Annexin V/PI staining. Results: The MTS assay revealed that cellular activity decreased after arctigenin treatment in a concentration-dependent manner (IC 50 = 4 µM). To investigate apoptosis induction, activity assays of caspase 3/7, 8, and 9 were performed. While caspase 3/7 and 8 exhibited high activity, caspase 9 showed no activity. Thus, apoptosis induction may have involved the action of tumor necrosis factor receptor 1 (TNFR1). Flow cytometry conducted with Annexin V/PI staining revealed the occurrence of early apoptosis. Conclusion: We found that arctigenin has anti-tumor effects in HUH-6 cells in a concentration-dependent manner. Arctigenin may have exerted its anti-tumor effect by inducing apoptosis via TNFR1, which recruits Complex IIa to activate caspase 8 and 3/7. These results may be useful for developing therapeutic agents for hepatoblastoma.

Original languageEnglish
JournalPediatric Surgery International
Publication statusAccepted/In press - 2019

All Science Journal Classification (ASJC) codes

  • Pediatrics, Perinatology, and Child Health
  • Surgery


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