POU6F1 inhibits cervical cancer progression by activating MAOB to block the ERK1/2 pathway

Cervical cancer (CC) ranks as the fourth common malignancy among women. This study investigated the mechanism by which POU6F1 mediates CC progression through MAOB.

MAOB expression was detected in CC tissues and cell lines. The effects of MAOB overexpression on cell proliferation, migration, and invasion were observed using CCK-8, EdU, colony formation, wound healing, and Transwell assays. Western blot was conducted to assess the extent of ERK1/2 phosphorylation. CC cell lines were treated with an ERK1/2 phosphorylation activator based on OE-MAOB to verify the effects of the ERK1/2 phosphorylation activator on CC cell growth. Transcription factors binding to the MAOB promoter were predicted. POU6F1 expression in cells was detected. Gene interference of OE-POU6F1 was performed, and the transcriptional relationship between POU6F1 and MAOB was confirmed through dual-luciferase and ChIP experiments. Based on OE-POU6F1, MAOB was knocked down to verify that POU6F1 affected CC development via MAOB in vitro and in vivo.

MAOB was downregulated in CC tissues (versus adjacent tissues) and cell lines (versus human cervical epithelial cells). MAOB overexpression repressed the proliferation, migration, and invasion of CC cells and suppressed the phosphorylation of ERK1/2. Treatment with an ERK1/2 phosphorylation activator weakened the repressive effect of MAOB overexpression on CC cell growth. POU6F1 was poorly expressed in CC cells, and POU6F1 transcriptionally activated MAOB. Combined knockdown of MAOB reversed the inhibited cell behaviors and tumor growth observed when POU6F1 was overexpressed alone.

POU6F1 inhibits CC progression by activating MAOB transcription and suppressing the ERK1/2 signaling activation.