miR-21 inhibitor suppresses cell proliferation and colony formation through regulating the PTEN/AKT pathway and improves paclitaxel sensitivity in cervical cancer cells

The present study aimed to investigate the role and the molecular mechanisms underlying the effects of microRNA-21 (miR-21) on the proliferation, apoptosis and colony formation of cervical cancer cells, and to examine the role of miR-21 in mediating the sensitivity of cervical cancer cells to paclitaxel (PTX). Reverse transcription-quantitative polymerase chain reaction was employed to determine the level of miR-21 in various cervical cancer and normal cervical cells. The results revealed that the expression levels of miR-21 in cervical cancer cells were markedly higher when compared with normal cervical cells. Subsequently, a miR-21 inhibitor or negative control (NC) was transfected into cervical cancer cells. Cell viability, colony formation and apoptosis were then analyzed using an MTT assay, crystal violet and Annexin V-fluorescein isothiocyanate/propidium iodide staining, respectively. The protein expression level of B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X (Bax), programmed cell death 4 (PDCD4), survivin, c-myc, phosphatase and tensin homolog (PTEN) and phosphorylated (p)-AKT were determined by western blot analysis. The sensitivity of cervical cancer cells to PTX (25, 50 and 100 mu g/ml) was characterized using an MTT assay. The results demonstrated that the miR-21 inhibitor promoted apoptosis of cervical cancer cells and suppressed their proliferation and colony formation when compared with the NC. In addition, the expression levels of Bcl-2, survivin, c-myc and p-AKT were significantly down-regulated in cells transfected with the miR-21 inhibitor, whilst the expression levels of Bax, PDCD4 and PTEN were significantly upregulated. Furthermore, the miR-21 inhibitor significantly enhanced the inhibition efficacy of PTX at a range of concentrations in cervical cancer cells. It was concluded that inhibition of miR-21 suppressed cell proliferation and colony formation through regulating the PTEN/AKT pathway, and improved PTX sensitivity in cervical cancer cells. The results of the present study may contribute to the development of miRNA-based cervical cancer therapy in the future.