Sufentanil inhibits the metastasis and immune response of breast cancer via mediating the NF-κB pathway.

Objective: Breast cancer (BC) causes cancer-related death in women. Sufentanil is used for cancer pain and postoperative analgesia. This study aimed to explore the role of sufentanil in BC.

Methods: BC cells were treated with sufentanil, and cell viability was evaluated using the cell counting kit-8 (CCK-8) assay. Biological behaviors were analyzed using EDU assay, flow cytometry, transwell assay, western blotting, and ELISA. The levels of NF-κB pathway-related factors were examined using western blotting. A xenograft tumor model was established to assess the effects of sufentanil on tumor growth in vivo.

Results: Sufentanil at the concentration of 20, 40, 80, and 160 nM suppressed cell viability (IC50 = 39.84 in MDA-MB-231 cells, and IC50 = 47.46 in BT549 cells). Sufentanil inhibited the proliferation, invasion, epithelial-mesenchymal transition (EMT), and inflammation, but induced apoptosis of BC cells. Mechanically, sufentanil suppressed the activation of the NF-κB pathway. Rescue experiments showed that RANKL (NF-κB receptor agonist) abrogated the effects induced by sufentanil. Moreover, sufentanil inhibited tumor growth, inflammatory response, but promoted apoptosis via the NF-κB pathway in vivo.

Conclusions: Sufentanil decelerated the progression of BC by regulating the NF-κB pathway, suggesting sufentanil may be used in BC therapy.