Exogenous interleukin-1 beta promotes the proliferation and migration of HeLa cells via the MEK/ERK signaling pathway

Objective Interleukin-1 beta (IL-1 beta) is a crucial cytokine that has been implicated in cancer and metastasis development. However, its possible mechanistic role in cervical cancer remains unclear. This study aimed to investigate the functions of exogenous IL-1 beta in cervical cancer cell proliferation and migration. Methods HeLa cell proliferation and migration were measured using MTT and Transwell assays. A lentivirus-mediated packaging system was used to construct an IL-1 beta overexpressing cell line. MEK/ERK signal transduction was inhibited by pretreatment with the MEK inhibitor PD98059. qRT-PCR and Western blotting were used to test the expression of relevant genes. Results Exogenous IL-1 beta promoted the proliferation and migration of HeLa cells. In addition, overexpression of IL-1 beta in HeLa cells promoted cell proliferation. Mechanistically, exogenous IL-1 beta increased the phosphorylated MEK and ERK levels in HeLa cells and the expression of JUN, RELB, and NF-kappa B2. Alternatively, blockade of MEK inhibited the promoting proliferation effects of IL-1 beta and the expression of JUN, RELB, and NF-kappa B2. Conclusions Our data suggest that exogenous IL-1 beta regulates HeLa cell functions by regulating the MEK/ERK signaling pathway and by targeting JUN, RELB, and NF-kappa B2. Our study uncovered a potential association across IL-1 beta, cervical tumor development, and cancer progression.