Seyma KIRMAN, Aylin AYDIN, Rüstem Anıl UĞAN
Meandros Medical and Dental Journal - 2026;27(3):481-490
Objective: Hepatocellular carcinoma (HepG2) is a leading cause of cancer-related mortality worldwide. Eritadenine has shown reduction in cell proliferation rates in various cancer cell models, while its role in wound healing remains unclear. This study evaluated the concentration-dependent dual effects of eritadenine on HepG2 cancer cells and L929 fibroblasts. Materials and Methods: HepG2 cells were treated with eritadenine (4x10?? - 4x10?? M) for 24, 48, and 72 hours. Cytotoxicity was determined using the MTT assay. For wound healing, confluent L929 fibroblasts underwent a scratch assay and were exposed to concentrations of 4x10?? - 4x10?? M. Wound closure was assessed microscopically at 24 and 48 hours. Although images were obtained up to 72 hours, quantitative analysis was performed only at 24 and 48 hours due to complete wound closure observed at later time points. Only commercially sourced cell lines were used, and no animal or human experiments were conducted. Results: High-dose eritadenine (4x10?? M) markedly reduced HepG2 viability at 24 hours, whereas the lowest dose (4x10?? M) enhanced proliferation at both 24 and 72 hours. Intermediate doses showed no significant changes. In fibroblasts, 4x10?? M induced the highest wound closure, while 4x10?? M also supported healing across both time points. Conclusion: Eritadenine exhibited concentration-dependent dual biological activity. High concentrations resulted in a significant reduction in HepG2 cell viability, whereas lower concentrations promoted fibroblast functions associated with the wound-healing process, leading to a marked increase in the wound closure rate. These findings suggest that eritadenine holds potential as a therapeutic candidate for both liver cancer research and tissue regeneration processes.
