miR-4306 inhibits the malignant behaviors of colorectal cancer by regulating lncRNA FoxD2-AS1

MicroRNA (miR)-4306 and FoxD2-adjacent opposite strand RNA 1 (FOXD2-AS1) are cancer-related genes involved in tumor progression. However, the potential functional roles of miR-4306 and FoxD2-AS1 in colorectal cancer (CRC) development remain unknown. The present study aimed to investigate the biological functions and the molecular mechanisms of miR-4306 and FoxD2-AS1 in CRC. Reverse transcription-quantitative PCR analysis was performed to determine the expression levels of FoxD2-AS1 and miR-4306 in CRC tissues and cell lines. Functional experiments, including Cell Counting Kit-8, colony formation, cell cycle assays and western blotting, were conducted to examine the effects of FoxD2-AS1 and miR-4306 on the malignant behaviors of CRC cells. In addition, the relationship between FoxD2-AS1 and miR-4306 was assessed using a dual-luciferase reporter assay and Pearson's correlation analysis. Compared with normal samples and cells, FoxD2-AS1 expression was increased and miR-4306 expression was decreased in CRC tissues and cells. Functional experiments demonstrated that silencing FoxD2-AS1 inhibited proliferation and induced cell arrest at G(0)/G(1) phase in CRC cells, while the overexpression of FoxD2-AS1 showed opposite results. Ki-67 and proliferating cell nuclear antigen expression levels were decreased after transfection with small interfering RNA FoxD2-AS1, but were increased after transfection with FoxD2-AS1 overexpression plasmid. Furthermore, investigations into the underling mechanism revealed that FoxD2-AS1 functioned as a molecular sponge of miR-4306. The inhibitory effects of FoxD2-AS1 silencing on CRC progression were reversed by miR-4306 knockdown. Collectively, the present study demonstrated that FoxD2-AS1 functioned as an oncogene in CRC progression, and that miR-4306 could inhibit the malignant behaviors of CRC by regulating FoxD2-AS1. Thus, the current study provided a promising therapeutic target for CRC treatment.