Objective  To explore the effect and mechanism of microRNA-135b (miR-135b) on apoptosis of HCT116 colon cancer cells.

  Methods   HCT116 cells were divided into control group, miR-135b NC group and miR-135b inhibitor group. Cell viability was detected with 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay. Cell apoptosis was detected with Hoechst staining. The expression of B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X (Bax), poly ADP-ribose polymerase (cleaved-PARP), cysteinyl aspartate specific proteinase (cleaved-caspase 3), phosphatase and tensin homolog deleted on chromosome ten (PTEN), phosphatidylinositol 3-kinase (PI3K), and protein kinase A (AKT) were detected with Western blot.

  Results  The expression of miR-135b was down-regulated in miR-135b inhibitor group compared with that in control group and miR-135b NC group (0.53 ± 0.05 vs. 1.00 ± 0.03 and 1.02 ± 0.04) (F = 259.19, P < 0.05). The cell viability and apoptotic rate of HCT116 cells were 0.58 ± 0.05 and 3.24 ± 0.13% for control group, 0.59 ± 0.06 and 3.27 ± 0.08% for miR-135b NC group, and 0.39 ± 0.04 and 36.48 ± 0.52% for miR-135b inhibitor group, respectively, with significantly decreased viability but increased apoptotic rate of HCT116 cells for miR-135b inhibitor group compared with that for control group and miR-135b NC group (both P < 0.05). Significantly down-regulated expressions of Bcl-2, cleaved-caspase 3, PI3K, and p-Akt and up-regulated expressions of Bax, cleaved-PARP, and PTEN were detected in miR-135b inhibitor group in comparison with those in control group and miR-135b NC group was (P < 0.05 for all).

  Conclusion   Dow-regulation of miR-135b could induce apoptosis of HCT116 cells, which might be related to the blocking of PTEN/PI3K/Akt signaling pathway.