miR‑410 regulates apoptosis by targeting Bak1 in human colorectal cancer cells

MicroRNAs (miRs) are essential in the pathogenesis of colorectal cancer (CRC). Previous studies have demonstrated that miR‑410 exerts multiple effects on tumors, however, whether it affects the apoptosis of CRC cells remains to be elucidated. In the present study, to demonstrate the role of miR-410 in CRC, miR-410 expression was detected in CRC tissues and cell lines, and the miR-410 level was manipulated by transfection with an miR-410 or miR-410 inhibitor in CRC cells. Cell growth and apoptosis was tested using an MTT assay, western blot and cytochrome C assay. Target validation was conducted by luciferase assay. It was found that miR‑410 was upregulated in CRC tissues and cell lines. The overexpression of miR‑410 resulted in an increase in growth activity and decrease in the extent of apoptosis. By contrast, the inhibition of endogenous miR‑410 activated the apoptotic machinery. Western blot analysis and a luciferase activity assay showed that Bak1 was directly targeted by miR‑410, and that knockdown of Bak1 attenuated the pro‑apoptotic effect of miR‑410 inhibition. In addition, it was shown that the expression of Bak1 was downregulated in CRC tumor tissues and was reversely correlated with the expression of miR‑410, which provided further support that Bak1 was regulated by miR‑410. The results of the present study suggested that miR‑410 may function as an oncogenic miR by suppressing the basal level of apoptosis. These findings may assist in understanding the molecular mechanisms of cancer development.