Objective To explore the effect of dexmedetomidine (Dex) on the malignant biological behaviors of endometrial cancer cells and its mechanism based on the Toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88) signaling pathway.

Methods The human endometrial cancer cell line Ishikawa was selected and divided into control group (conventional culture), low-dose Dex group (with the addition of 10 nmol/L Dex), medium-dose Dex group (with the addition of 20 nmol/L Dex), and high-dose Dex group (with the addition of 40 nmol/L Dex). The CCK-8 method and flow cytometry were used to detect the cell proliferation activity and apoptosis rate of each group. Transwell invasion assay and cell scratch assay were employed to evaluate the invasion and migration abilities of the cells in each group. A subcutaneous xenograft nude mouse model was constructed to assess the tumor-forming ability of each group, and the Western blot was used to detect the expression of TLR4 and MyD88 proteins in the tumor tissues of the nude mice in each group.

Results Compared with the control group, the proliferation activity, invasion ability, and migration ability of Ishikawa cells in the low-dose, medium-dose, and high-dose Dex groups were all decreased, showing a dose-dependent downward trend with the increase in Dex concentration, and the differences were statistically significant (P < 0.05). Compared with the control group, the apoptosis rates of the cells in the low-dose, medium-dose, and high-dose Dex groups were all increased, showing a dose-dependent upward trend with the increase in Dex concentration, and the differences were statistically significant (P < 0.05). Compared with the control group, the volume and mass of the subcutaneous xenograft tumors in the nude mice of the low-dose, medium-dose, and high-dose Dex groups were all reduced, and the relative expression levels of TLR4 and MyD88 proteins in the tumor tissues were all decreased, showing a dose-dependent downward trend with the increase in Dex concentration, and the differences were statistically significant (P < 0.05).

Conclusion Dex can inhibit the invasion and migration of endometrial cancer cells and induce cell apoptosis, and its mechanism of action may be related to the inhibition of the TLR4/MyD88 signaling pathway.