MicroRNA-889 promotes cell proliferation in colorectal cancer by targeting DAB2IP.

Abstract

Colorectal cancer (CRC) remains one of the most frequent lethal malignant tumors worldwide. The correlation between miR-889 expression and CRC progression has not been well identified in the recent literature. Here, we aim to detect the role and mechanism of miR-889 in CRC. First, miRNA RT-PCR (Real Time-Polymerase Chain Reaction) was performed to determine miR-889 expression in CRC tissues and cells. The proliferative capacity of cells transfected with miR-889 mimics, miR-889 inhibitor or NC was measured by CCK-8 (cell counting kit-8), colony formation and EdU (5-Ethynyl-2'-deoxyuridine) assays. The online bioinformatics sites were chosen to predict possible downstream regulatory genes of miR-899. The dual-luciferase report assay was conducted to verify the relation between DAB2IP (DAB2 interacting protein) and miR-899. The expression changes of DAB2IP were assessed by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) and Western blot. MiR-889 was upregulated in CRC tissues and CRC cells, and upregulated miR-889 was confirmed to promote cell growth in vitro. Dual-luciferase reporter, qRT-PCR, and Western blot assays suggested that DAB2IP might be regulated by miR-889. The effects of miR-889 on proliferation could be abolished by DAB2IP through confirmatory experiments. By directly targeting DAB2IP, miR-889 served as a vital part in accelerating CRC cell proliferation. Our current study substantiated that miR-889 might participate in controlling CRC proliferation by regulating DAB2IP, which provides potential and prospective therapeutic target for CRC.