Remifentanil induces apoptosis and G1-phase cell cycle arrest in human MCF-7 breast cancer cells

Abstract

Objectives: Remifentanil, a fentanyl-derivative opioid analgesic acting as a μ-opioid receptor agonist, is a crucial drug in anesthesia due to its numerous benefits during surgical procedures. This study aimed to explore whether remifentanil effectively induced apoptosis in MCF-7 breast cancer cells via possible mechanisms. Methods: Flow cytometry was performed for Annexin V/7-aminoactinomycin (7-AAD) and DAPI staining, cell cycle assays, and to measure reactive oxygen species (ROS) levels. Immunoassays for lactate dehydrogenase (LDH) and interleukin (IL)-6, as well as a chorioallantoic membrane (CAM) test, were also performed. Results: Remifentanil effectively suppressed cell proliferation and led to the induction of cell cycle arrest at the G1 phase in MCF-7 cells. Compared with the control group, MCF-7 cells treated with remifentanil had a higher apoptotic rate with nuclear fragmentation, increased LDH release, and lower IL-6 concentrations. Overgeneration of ROS and decreased angiogenic activity were also observed in remifentanil-treated MCF-7 cells. Conclusion: Remifentanil led to G1-phase arrest and apoptosis in MCF-7 cells. The mechanism of action of remifentanil likely involves the suppression of IL-6 production and angiogenesis, along with enhanced ROS levels and LDH generation. This preliminary study highlighted the need for further experimental evidence from future research to clearly support the significant potential of remifentanil as an anticancer agent for breast cancer. Keywords: Anticancer effect, apoptosis, MCF-7 breast cancer cells, oxidative stress, remifentanil