Restoring lost function to suppressor gene products has captured the interest of the research community in the field of gene therapy. , also known as , is a tumor suppressor gene, and its deregulation may be responsible for cancer progression. The aim of this study was to investigate whether mRNA has an anti-cancer function by regulating onco-miRNA expression in colorectal cancer (CRC) cells. miRNAs targeting were predicted by bioinformatics analysis and further confirmed by dual-luciferase reporter assays and RT-qPCR. The altered expression of microRNA was validated in early-stage CRC tumor tissues by miRseq. Cell proliferation was measured by Cell Counting Kit-8 (CCK-8) assay. Cell invasion and migration were detected by transwell and wound healing assays, respectively. In vivo experiments were conducted to confirm the in vitro findings. Among all miRNAs, reversed correlation between expression and miRNA-183-5p expression was most significant. Luciferase assays revealed that directly targeted miR-183-5p. The miRseq data showed that miR-183 was also dysregulated at the early stage of tumor development and upregulated in late sub-stage II CRC patients ( <0.01). Mechanistic analysis both in vitro and in vivo demonstrated that anti-miR-183-5p depressed cell proliferation, migration, and invasion in CRC cells while miR-183-5p overexpression resulted in opposite effects. Our findings suggested that oncomiR-183-5p promoted the proliferation, migration, and invasion of CRC cells. miRNA-binding elements (MREs) suppressed miRNA-183-5p activities. Any change in expression of thus affected miRNA-183-5p. This may be another anti-tumor mechanism in addition to protein-mediation that regulates tumor suppressor genes.