Papillary thyroid carcinoma (PTC) is primarily managed through surgical intervention, underscoring the importance of understanding the biological effects of anesthetic agents used during such procedures. Dexmedetomidine is a widely used clinical anesthetic; however, its direct effects on PTC cells and the underlying mechanisms remain unclear. This study combined bioinformatic analysis and in vitro experiments to investigate these mechanisms. We identified 25 potential dexmedetomidine targets in PTC through database screening and further identified 10 hub genes. GO and KEGG enrichment analyses indicated that these genes were significantly involved in the MAPK signaling pathway, among others. In vitro experiments showed that dexmedetomidine, at micromolar concentrations, inhibited cell proliferation and migration, induced apoptosis, and caused G2/M phase arrest in a concentration-dependent manner. Mechanistic investigations revealed that dexmedetomidine concurrently activated the p38 MAPK pathway and suppressed PI3K/Akt signaling. Rescue experiments confirmed that inhibition of p38 reduced its pro-apoptotic effect, whereas activation of Akt reversed its anti-proliferative activity. These findings demonstrate, in an in vitro model, that dexmedetomidine suppresses malignant behaviors in PTC cells through synergistic regulation of the p38 MAPK and PI3K/Akt signaling pathways, providing novel mechanistic insights into its pleiotropic effects. Nevertheless, translating these in vitro findings into clinical practice warrants further investigation.
Sun et al. (Fri,) studied this question.