Colorectal carcinoma (CRC) is a malignant solid tumor arising from the large intestine and is associated with an increasing incidence and poor prognosis. Further understanding of the molecular mechanisms underlying CRC may contribute to the development of novel effective therapeutic strategies. MicroRNAs (miRs), including miR-155, have been reported to be associated with the etiology and biology of CRC; however, the molecular mechanisms by which miR-155 affect CRC remain to be fully elucidated. The present study used a multidisciplinary approach, involving reverse transcription-quantitative polymerase chain reaction, northern blotting, MTT assay, cell cycle progression analysis, immunoblotting, and animal experiments, to determine the possible targets of miR-155 in CRC cells. miR-155 was found to be overexpressed in CRC tissue samples, compared with paired normal colon tissue samples. In addition, the inhibition of miR-155 induced a deceleration in CRC cell proliferation and inactivation of the Wnt/-catenin signaling pathway. miR-155 suppression also reduced the growth of CRC xenografts in an animal model. HMG-box transcription factor 1 (HBP1) was identified as a novel target of miR-155, which mediated its effect on CRC via the Wnt/-catenin pathway. Furthermore, patients with CRC exhibiting higher serum levels of miR-155 exhibited reduced survival rates. In conclusion, the present study demonstrated that miR-155 may contribute to the progression and growth of CRC by enhancing the Wnt/-catenin pathway in an HBP1-associated mechanism. Therefore, miR-155 may be considered a promising therapeutic target for the treatment of CRC.