Lycorine induces cell-cycle arrest in the G0/G1 phase in K562 cells via HDAC inhibition

Li, Lv; Dai, Hong-Juan; Ye, Mao; Wang, Shu-Ling; Xiao, Xiao-Juan; Zheng, Jie; Chen, Hui-Yong; Luo, Yu-hao; Liu, Jing

HATs and HDACs regulate the chromatin structure and gene transcription. Their dynamic balance plays a crucial role in various biological functions, including cell proliferation and death. Their dysregulation has been related to the development and progression of various cancers, including forms of myeloid leukemia [13, 14] . Recent studies have utilized HDACs as a promising target enzyme in anticancer drug development. Several studies have shown that HDAC inhibitors can induce differentiation of tumor cells, arrest the cell cycle at the G0/G1 phase, and activate the cell apoptosis gene. Normal cells are relatively resistant to HDAC inhibitor-induced cell death [15, 16] . The results of our study reveal that lycorine inhibits the activity of HDACs but does not affect their expression in K562 cells, which indicates that lycorine is a promising potential therapy agent in CML. However, the detailed molecular mechanism behind the inhibition of HDAC enzymatic activity by lycorine must be investigated further.