Emodin exerts antitumor effects in cervical cancer cells by reprogramming phospholipid metabolism through modulation of H3K27ac and H3K27me3
Emodin, a natural compound derived mainly from Reynoutria japonica (Huzhang), has demonstrated notable antitumor effects, though its epigenetic regulatory mechanisms in cervical cancer remain largely unclear. In this study, we show that emodin suppresses cervical cancer cell proliferation and induces oxidative stress. Integrated transcriptomic and metabolomic analyses further demonstrated that emodin markedly disrupted lipid metabolism, particularly by increasing phospholipid accumulation and promoting phospholipid peroxidation. Epigenetic profiling using Western blotting showed that emodin treatment altered global histone modification patterns, with notable increases in H3K27ac and H3K27me3 levels. Subsequent CUT&Tag analysis combined with ChIP-qPCR validation indicated that emodin modulates these two histone marks to regulate the transcription of key phospholipid metabolism-related genes, thereby contributing to enhanced phospholipid peroxidation and antitumor activity. Together, these findings provide new insights into the epigenetic antitumor mechanisms of emodin and highlight potential histone modification targets involved in phospholipid metabolism.