Abstract
Ropivacaine, one of the most commonly used local anesthetics in clinical practice, has shown potent antitumor activity in multiple types of cancer cells. However, its effect on cervical cancer cell growth remains unknown. In the present study, it was found that ropivacaine inhibited cervical cancer cell growth by suppressing cell cycle progression and promoting cell apoptosis, as determined by CCK‑8 assay, cell cycle and apoptosis analyses. Western blot analysis and luciferase assay demonstrated that ropivacaine abrogated the phosphorylation and transcriptional activation of signal transducer and activator of transcription 3 (STAT3), and that STAT‑3C overexpression reversed the inhibition of cervical cancer cell viability mediated by ropivacaine. Furthermore, our results revealed that the increased expression of maternally expressed gene 2 (MEG2) caused by ropivacaine led to STAT3 dephosphorylation. Finally, we found that ropivacaine upregulated MEG2 by decreasing the expression of microRNA‑96 (miR‑96). Taken together, our results describe a novel mechanism for the anticancer activity of ropivacaine and suggest ropivacaine as a potential therapeutic agent for cervical cancer patients.