miR-592, as a potential biomarker, has been linked to several cancers. However, the expression level and prognostic value of miR-592 in CRC have not been elucidated. In this study, we detected the miR-592 expression in CRC serum, tumor tissues, adjacent non-tumor tissues (NATs) and four colorectal cancer cell lines by RT-PCR. Our data proved that miR-592 expression was up-regulated in clinical CRC serum and tissues (P<0.05). Serum or tissue miR-592 in CRC metastatic patients also maintained a high level, compared to that in non-metastatic CRC patients (P<0.05). After radical surgery, postoperative serum miR-592 level in CRC patients significantly decreased (P<0.05). Our clinicopathological analysis revealed that high miR-592 was significant associated with the tumor size (P=0.008), TNM stage (P=0.026), distant metastasis (P=0.004) and preoperative CEA level (P=0.022), which led to a shorter overall survival rate in CRC patients (P=0.032). Furthermore, we designed and transfected miR-592 mimics or inhibitors into the corresponding CRC lines, and our experiments in vitro demonstrated that miR-592 could promote cell proliferation, wound healing and invasion ability of CRC cells (P<0.05), while miR-592 did not influence the CRC cell apoptosis (P>0.05). All these results suggested that miR-592 functioned as a novel and potential carcinogen-initiated and metastasis-related biomarker in CRC, and down-regulation of miR-592 might be considered as a potentially significant molecular treatment strategy for CRC patients.