Silencing of inhibits human cervical cancer through the AKT signaling pathway.

BACKGROUND

has been demonstrated to be highly expressed in various human cancers including cervical cancer, and has been shown to play a critical role in tumor aggressiveness. We aimed to investigate the role of in human cervical cancer in vitro and in vivo.

METHOD

Reverse transcription-quantitative polymerase chain reaction assay and Western blot assay were used to detect the mRNA and protein expression, respectively. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and were performed to measure the viabilities of cancer cells. Flow cytometry assay was used to detect the cell cycle and apoptosis. Moreover, an animal experiment was performed to evaluate the biological behavior of in vivo.

RESULTS

In the current study, we found that was obviously over-expressed in cervical cancer tissues compared to the adjacent non-cancer tissues. Cervical cancer cells transfected with siRNA demonstrated significant inhibition of cancer proliferation ( < 0.01), cell cycle arrest at G0/G1 phase, and cell apoptosis ( < 0.05). Moreover, down-regulation of significantly inhibited cervical cancer growth in vivo. In addition, protein levels of , c-Myc and Cyclin D1 were much lower in the siRNA-treated groups than that in the control group.

CONCLUSIONS

inhibition reduced cervical cancer tumor growth through the AKT pathway. This effect represented a therapeutic opportunity and provided a novel target for cervical cancer treatment.