Background: MicroRNAs influence almost every genetic pathway and are involved in colorectal cancer (CRC). However, the biological role of miR486-3p in CRC remains to be elucidated. Methods: In this study, miR486-3p expression in CRC cell lines and normal colonic epithelial cells was determined. After miR486-3p mimic, inhibitor, and BIK siRNA transfection, cell proliferation, apoptosis, and migration were examined. Furthermore, the target of miR486-3p was identified by luciferase-reporter assay and underlying molecular mechanisms studied. Results: The results revealed that miR486-3p was significantly upregulated in CRC compared with normal colonic epithelial cells, whereas BIK expression was remarkably downregulated in CRC cells. MTT assays demonstrated that suppression of miR486-3p expression reduced CRC cell proliferation, whereas elevated miR486-3p or BIK silencing induced cell proliferation. Woundhealing assays and transwell experiments revealed that both upregulation of miR486-3p and down-regulation of BIK increased CRC cell migration and invasion ability. Moreover, bioinformatic target prediction identified BIK as a putative target of miR486-3p. Knockdown of miR486-3p was shown to upregulate BIK expression, whereas overexpression of miR486-3p suppressed the expression of BIK. Luciferase reporter assay results further confirmed this deduction. Conclusion: In conclusion, these findings suggest that miR486-3p is an oncogene in CRC. Gene therapy using miR486-3p inhibition may provide a new clue for CRC therapy.