mir-106a regulates cell proliferation and apoptosis of colon cancer cells through targeting the PTEN/PI3K/AKT signaling pathway.

Colorectal cancer (CRC) is a common digestive tract tumor. Cancer tissues and healthy tissues were extracted from patients with CRC who were treated at our hospital. Targetscan and PicTar were used to identify microRNAs (miRNAs/miRs) that may interact with phosphatase and tensin homolog deleted on chromosome ten (PTEN). Dual luciferase reporter assay was applied to detect whether the 3'-untranslated region (UTR) of PTEN was targeted by miR-106a. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) showed that there was significantly higher miR-106a expression level in cancer tissue compared with in healthy tissue. The expression level of miR-106a in NCM640, SW620 and HT29 cell lines was detected by RT-qPCR, and HT29 cells showed the highest miR-106a level. HT29 cells were used for the present study, separated into control, miR-NC antagomiR and miR-106a antagomiR group. HT29 cell characteristics were tested. The results demonstrated that in the miR-106a antagomiR group, there was a lower cell proliferation and higher cell apoptosis rate compared with the control and miR-NC antagomiR groups. miR-106a was verified to target PTEN 3'-UTR in HT29 cells. In comparison with control and miR-NC antagomiR groups, the protein level of PTEN was increased and phosphatidylinositol-4,5-bisphosphate 3-kinase/protein kinase B was decreased following miR-766 antagomiR administration. The findings propose that miR-106a may serve a therapeutic target for the treatment of CRC.