Long non-coding RNA-PCGEM1 contributes to prostate cancer progression by sponging microRNA miR-129-5p to enhance chromatin licensing and DNA replication factor 1 expression

PCGEM1 facilitates prostate cancer (PCa) progression. This study aimed to elucidate the mechanism of action of PCGEM1 in PCa. The expression of PCGEM1, microRNA miR-129-5p, chromatin licensing, and DNA replication factor 1 (CDT1) was detected by quantitative reverse transcription-PCR (qRT-PCR). A series of function experiments including cell counting kit-8 (CCK-8), caspase-3 activity, and cell cycle assays were performed to evaluate the influence of PCGEM1, miR-129-5p, and CDT1 on the biological processes of PCa cells. CyclinD1, cyclin dependent kinase 4 (CDK4), Bax, and Bcl-2 protein levels were measured by western blotting. Subcellular isolation revealed the distribution of PCa cells. The connections between PCGEM1, miR-129-5p, and CDT1 were evaluated by luciferase, RIP assay, and Pearson correlation analysis. Both PCGEM1 and CDT1 were upregulated in PCa, while miR-129-5p was downregulated and negatively correlated with PCGEM1 and CDT1. Downregulation of PCGEM1 or CDT1 inhibited the viability, promoted apoptosis and cycle arrest of PCa cells <i>in vitro</i>, and controlled tumor growth <i>in vivo</i>. PCGEM1 plays a crucial role in the progression of PCa by sponging miR-129-5p as a ceRNA of CDT1. PCGEM1 is a CDT1-dependent PCa promoter site that absorbs miR-129-5p.