Mechanistic insights into the effect of midazolam on the malignant progression of ovarian cancer.

Objective: As the first gynecological tumor, ovarian cancer seriously threatens women's lives and health. Here, the possible mechanism of midazolam against ovarian cancer progression was investigated. Material and Methods: OVCAR3 and SKOV3 cells were treated with midazolam for 24 h, and cell activity was subsequently detected by cell counting kit-8 assay to screen for the suitable treatment concentrations of midazolam. Cell proliferation was investigated through 5-ethynyl-2'-deoxyuridine staining and cell plate cloning experiments. Apoptosis rate was detected by flow cytometry, and cell invasion and migration ability were examined through transwell test and scratch test. Western blot was adopted to explore the expression changes of apoptotic proteins, cell cycle-related proteins, and extracellular signal-regulated kinase/c-Jun N-terminal kinase (ERK/JNK) pathway-related proteins. Results: After midazolam intervention, the OVCAR3 and SKOV3 cells showed decreased proliferation, invasion, and migration abilities and accelerated apoptosis rate. Western blot results displayed that midazolam downregulated the phosphorylation levels of ERK, JNK, and P38. Anisomycin reversed the effect of midazolam on the ERK/JNK pathway and cell proliferation, apoptosis, cell cycle, invasion, and migration. Conclusion: Midazolam can block the development of ovarian cancer, and the relevant mechanism may be realized through the ERK/JNK pathway.