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Cancer metastasis and recurrence are major causes of poor survival in patients with colorectal cancer (CRC). Therefore, the biological behavior of microRNA (miR)‑451 in CRC deserves further investigation. Reverse transcription‑quantitative PCR was applied to measure the relative expression of miR‑451 in blood serum specimens from patients with CRC and CRC cells. In vitro , HCT116 cells were transfected with miR‑451 mimics, a miR‑451 inhibitor, or SAMD4B plasmids. Proliferation, migration and apoptosis were measured using CCK‑8, Transwell assays and flow cytometry, respectively. Luciferase reporter assay was used to identify targets of miR‑451 and western blotting performed to explore the internal mechanisms of miR‑451 regulation. In vivo , the effect of miR‑451 and SAMD4B plasmids on tumor growth was analyzed using a nude mouse xenograft model. Results indicated that serum miR‑451 expression was lower in patients with CRC compared with healthy controls. Patients with elevated expression of miR‑451 had longer survival times compared with those with low expression. Overexpression of miR‑451 inhibited proliferation and migration, promoted apoptosis and enhanced the sensitivity of CRC cells to chemotherapy. SAMD4B was identified as a direct target of miR‑451 using miRNA target prediction programs and dual luciferase reporter assay validated the binding site of miR‑451 in the 3‑'UTR region of SAMD4B. Further studies confirmed that miR‑451 inhibited CRC progression via targeting SAMD4B. Results indicated that miR‑451 is essential for blocking tumor growth via targeting SAMD4B in vivo and in vitro . The miR‑451/SAMD4B axis may serve as a novel therapeutic target in patients with CRC.

miR‑451 suppresses the malignant characteristics of colorectal cancer via targeting SAMD4B