H3K27ac-induced lncRNA PAXIP1-AS1 promotes cell proliferation, migration, EMT and apoptosis in ovarian cancer by targeting miR-6744-5p/PCBP2 axis

We aimed to explore role of lncRNA PAX-interacting protein 1-antisense RNA1 (PAXIP1-AS1) in ovarian cancer (OC). RT-qPCR analysis identified upregulation of PAXIP1-AS1 in OC cell lines. Functionally, PAXIP1-AS1 knockdown inhibited cell proliferation, accelerated cell apoptosis, and suppressed cell migration and epithelial-mesenchymal transition (EMT) process. Upregulation of PAXIP1-AS1 was induced by CBP-mediated H3K27 acetylation (H3K27ac) via bioinformatic analysis and ChIP assay. Furthermore, PAXIP1-AS1 served as a competing endogenous RNA (ceRNA) to regulate PCBP2 expression by sponging microRNA-6744-5p (miR-6744-5p). Restoration experiments showed that overexpressed PCBP2 rescued effects of silenced PAXIP1-AS1 on cell proliferation, apoptosis, migration and EMT. Overall, lncRNA PAXIP1-AS1 activated by H3K27ac functioned as a tumor promoter in OC via mediating miR-6744-5p/PCBP2 axis, which provided promising insight into exploration on OC therapy.

Automated summary

PAXIP1-AS1, activated by H3K27ac, functions as a tumor promoter in ovarian cancer by mediating the miR-6744-5p/PCBP2 axis to regulate cell proliferation, apoptosis, migration, and EMT.