Long non-coding RNA POC1B-AS1 depletion represses colorectal cancer progression through the microRNA-625-5p/FOXK1 axis.

OBJECTIVES: Numerous long non-coding RNAs (lncRNAs) are aberrantly expressed in colorectal cancer (CRC), causing its high aggressiveness and uncontrolled growth. Therefore, exploring the regulatory activities of lncRNAs in CRC could facilitate the development of promising therapeutic targets. This study aimed to illustrate the role of POC1B antisense RNA 1 (POC1B-AS1) in CRC malignancy. METHODS: POC1B-AS1 expression levels were quantified by quantitative real-time polymerase chain reaction. Its biological roles were investigated through functional experiments. Luciferase reporter and RNA immunoprecipitation assays were employed to illustrate the underlying mechanisms. RESULTS: Highly expressed POC1B-AS1 in CRC was confirmed. Depletion of POC1B-AS1 resulted in reduced proliferative, colony formative, migratory and invasive capacities of CRC cells in vitro, and suppressed tumor growth in vivo. POC1B-AS1 functioned as a sponge for microRNA-625-5p (miR-625-5p), and consequently overexpressed forkhead box K1 (FOXK1) expression in CRC. Additionally, the repressing actions of POC1B-AS1 ablation on CRC cell aggressiveness were attenuated due to miR-625-5p downregulation or FOXK1 overexpression. Ablation of POC1B-AS1 inhibited the malignant progression of CRC cells by sequestering miR-625-5p and thereby up-regulating FOXK1. CONCLUSIONS: Our study suggest that the manipulation of POC1B-AS1/miR-625-5p/FOXK1 pathway-mediated aggressiveness in CRC may offer an effective therapeutic target.