Abstract: Objective To investigate the effect of miR-93 and the sensitivity of colon cancer HT-29 cells on 5-FU and its possible mechanism. Methods  miR-93 inhibitor was transfected into HT-29 cells， and blank control group and negative control group （NC） were also set up. Cell proliferation was detected by MTT assay. The apoptosis， invasion and migration activities of HT-29 cells in the miR-93 inhibitor group， blank control group and NC group were detected by flow cytometry， Transwell cell invasion test and scratch test respectively. Double luciferase reporter gene method was used to verify the relationship between PTEN and miR-93. Real-time fluorescence quantitative PCR （QPCR） was used to detect the expression of miR-93 and the effect on the expression of p-VEGFR2， p-Akt and PTEN mRNA in the three groups. Results The relative expression of miR-93 in the miR-93 inhibitor group was 0.40±0.05， significantly lower than that in the blank control group and NC group （1.13±0.08，1.12±0.09）， and the difference was statistically significant （P＜0.05）. The proliferation inhibition rate of HT-29 cells treated with 1， 4， 16， 64， 256 μg／ml 5-FU in miR-93 inhibitor group was higher than that in the NC group and the blank control group （P＜0.05）. The apoptosis rate， invasion rate and healing rate of HT-29 cells treated with 16 μg／ml 5-FU in the inhibitor group were （52.75 ±7.44）％， （45.76 ±15.85）％， （12.64 ±3.29）％ respectively， which were significantly different from those in the control group and NC group （P＜0.05）. PTEN might be a target protein of miR-93 which was verified by the dual luciferase reporter gene system. The expression levels of p-VEGF R2， p-Akt and PTEN in HT-29 cells treated with inhibitor of miR-93 were 1.28±0.09，0.85±0.08 and 1.22±0.09， respectively. Compared with control group and NC group， the phosphorylation levels of VEGFR2 and Akt were down-regulated and the expression of PTEN was up-regulated. Conclusion Down-regulation of miR-93 can increase the expression of PTEN， inhibit the phosphorylation of VEGFR-2 and Akt， and thus enhance the sensitivity of colon cancer cells to 5-FU.

Key words: Colon cancer, microRNAs, 5-FU, Sensitivity, PTEN