Imiquimod inhibits U87 cell proliferation and migration in vitro through inhibition of STAT-3 NF-kB signalling pathway

Imiquimod, known for its immune-modulating properties, has emerged as a potential anti-cancer agent. The U87 glioblastoma cell line, known for its high malignancy and poor prognosis, presents a significant challenge in neuro-oncology. Targeting the STAT-3/NF-?B pathways offers a promising therapeutic strategy for glioblastoma treatment. Imiquimod potentially inhibits these oncogenic signaling routes to suppress U87 cell proliferation and migration. We investigated the effect of imiquimod (IMQ) on U87 cell growth using CCK-8 and cell scratch assays. Western blotting analyzed protein levels of STAT-3, p-STAT-3, NF-?B, and p-NF-?B, while flow cytometry assessed U87 cell apoptosis rates. ELISA detected cellular inflammatory factor levels. In vivo experiments further evaluated IMQ's impact on U87 cell growth. Findings suggest that IMQ suppresses U87 cell growth and movement, inhibits STAT-3 and NF-?B phosphorylation, and accelerates apoptosis. ELISA assays indicated that IMQ reduced local inflammation. Adding a STAT-3 inhibitor yielded similar effects to IMQ, altering cell proliferation, migration, and apoptosis. Overall, IMQ appears to inhibit U87 cell proliferation and migration, inducing programmed cell death through STAT-3 modulation.