Objective To explore the molecular mechanism of DPY30-mediated H3K4 methylation promoting PCNA expression to promote colorectal cancer cell progression.

Methods The samples from colorectal cancer patients were collected, and the DPY30 expression was detected by immunohistochemistry. After the silencing DPY30 vector was constructed, the effects of silencing DPY30 on the proliferation and metastasis of colorectal cancer were detected by cell cloning assay, CCK-8 assay, 3D pellet forming assay and apoptosis assay. The interfering DPY30 to influence H3K4 histone methylation to reduce the expression was investigated using WB, and the expression of PCNA affected by interference of DPY30 were detected using the PCR and WB.

Results DPY30 was overexpressed in colorectal cancer (P ＜ 0.01) and correlated with poor pathological stage. The results of cell cloning experiment, CCK-8 experiment, 3D pellet forming experiment and apoptosis experiment showed that compared with NC group, the cell proliferation ability was inhibited, and the apoptosis increased in DPY30 group (P ＜ 0.05 to P ＜ 0.01). The results of Western blotting results showed that silencing DPY30 inhibited H3K4 methylation, while PCNA expression decreased (P ＜ 0.05 to P ＜ 0.01).

Conclusions DPY30 promotes PCNA expression by mediating H3K4 methylation, thus participating in colorectal cancer progression.