Furthermore, we found that the knockdown of ASH1L in PC3 cells induced more S arrest and decreased the fraction of the G0-G1 phase and G2-M phase than that in DU145 cells, suggesting that PC3 and DU145 likely have distinct mechanisms for CRPC tumor cell progression and PCa heterogeneity and that ASH1L may play a bigger role in the regulation of cell cycle in PC3 than in DU145 cells. Here, ASH1L is linked to neoplasm.