Recent advances in the antileukemic mechanisms of fucoidan based on epigenetic regulation (Review)

Leukemia is a malignant clonal disease originating from hematopoietic stem cells, whose complex pathogenesis is associated with multiple factors. Epigenetic regulation has been found to play an important role in the occurrence and development of leukemia, and has become a major focus of research. Fucoidan (FPS), a natural sulfated polysaccharide primarily extracted from marine brown algae, is rich in L‑fucose and sulfate groups. It has a variety of biological activities, including antioxidant, antiviral, immunomodulatory and antitumor activities. Notably, FPS exhibits antileukemic potential by epigenetically inhibiting the protein expression of DNA methyltransferases, regulating methylation levels at the promoter regions of specific genes such as peroxiredoxin 2, influencing the activity of histone‑modifying enzymes, and controlling the expression of non‑coding RNAs (ncRNAs), including microRNAs and long ncRNAs. These effects collectively suppress the proliferative and differentiation of leukemic cells. The present review examines the epigenetic regulatory mechanisms by which FPS may inhibit leukemia, including DNA methylation, histone modification and ncRNA‑associated mechanisms. In addition, it also discusses the potential advantages and challenges of FPS in the treatment of leukemia, as well as future research directions for FPS in leukemia therapy, aiming to provide a stronger theoretical basis for its clinical application.