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.