To elucidate the potential function of lncRNA CACS15 in the progression of ovarian cancer (OC) and its underlying mechanism. CACS15 level in OC tissues and cell lines was determined by qRT-PCR. Correlation between CACS15 level and survival of OC patients was analyzed through Kaplan-Meier method. Regulatory effects of CACS15 on cellular behaviors of OC cells were evaluated through CCK-8 and Transwell assay. Subsequently, RIP and RNA pull-down were performed to uncover the interaction between CACS15 and EZH2. Through ChIP assay, the interaction between EZH2 and APC was illustrated. A series of rescue experiments were finally conducted to elucidate the role of CACS15/APC axis in the malignant progression of OC. CACS15 was upregulated in OC tissues and cell lines relative to matched ones. High-level of CACS15 predicted worse survival in OC patients. Knockdown of CACS15 attenuated proliferative, migratory and invasive abilities of OC cells. CACS15 was mainly distributed in cytoplasm of OC cells, which was interacted with EZH2 at post-transcriptional level. Knockdown of CACS15 reduced the occupancies of EZH2 and H3K27me3 in APC promoter regions. Notably, knockdown of APC could reverse the regulatory effect of CACS15 on cellular behaviors of OC cells. LncRNA CACS15 inhibits the expression of APC by recruiting EZH2, thus accelerating the progression of ovarian cancer as an oncogene.