miR‑1 inhibits the progression of colon cancer by regulating the expression of vascular endothelial growth factor.

MicroRNA (miR)‑1 is associated with various human malignancies through repressing tumor growth, migration and angiogenesis. Recently, high‑throughput transcriptional profiling confirmed that miR‑1 is markedly downregulated in metastatic colorectal cancer; however, its biological functions and the specific underlying mechanisms in colorectal cancer (CRC) require further investigation. In this study, the expression of miR‑1 in 111 CRC and paired normal tissue samples was measured using quantitative polymerase chain reaction analysis, and the association between miR‑1 expression and clinical characteristics was evaluated. miR‑1 was found to be significantly downregulated in CRC tissues compared with paired normal tissues, and in CRC cell lines compared with non‑cancer cells (P<0.001), and was negatively associated with tumor size (P=0.001), differentiation (P=0.011), lymph node metastasis (P=0.001) and TNM stage (P=0.001). Further experiments revealed that miR‑1 inhibited the migration and invasion of HCT116 and ClonA1 cells, and inhibited cell proliferation by affecting the cell cycle. Vascular endothelial growth factor (VEGF) was found to be a potential target of miR‑1 by biological prediction, and further investigation confirmed that miR‑1 significantly inhibited the expression and paracrine function of VEGF. In CRC tissues, the expression of VEGF was negatively correlated with miR‑1. The low expression of miR‑1 in CRC may be one of the reasons for the abnormally high expression of VEGF; the upregulation of miR‑1 expression may inhibit cancer progression by downregulating VEGF. These findings indicate that treatment with miR‑1 may be a novel method of tumor suppression, and provide a theoretical and experimental basis for the further targeted treatment of CRC through the regulation of miR‑1 and VEGF expression.