Because of the characteristics of high invasiveness, relapse, and poor prognosis, the management of malignant gliomas has always been a great challenge. Nod-like receptor (NLR) family pyrin domain containing 3 (NLRP3) is a crucial component of the NLRP3 inflammasome, a multiprotein complex that can trigger caspase 1/interleukin-1 (IL-1)-mediated inflammatory response once activated and participates in the pathogeny of diverse inflammatory diseases as well as cancers. We examined the function of NLRP3 in the development of glioma. Glioma cells were treated with NLRP3 interference or overexpression vectors, recombinant IL-1 beta, IL-1 beta antibody, and NF-kappa B inhibitor. Cell proliferation and invasion were assessed by CCK-8 and Transwell assays. Gene expression was detected by PCR, Western blot, and ELISA. NLRP3 and NF-kappa B p65 increased and were positively correlated in glioma tissues. NLRP3 knockdown suppressed glioma cell growth and invasion with the decrease of IL-1 beta and NF-kappa B p65. Conversely, forced expression of NLRP3 promoted cell growth. NLRP3 silencing suppressed ectogenous IL-1 beta-elevated cell proliferation and invasion, whereas IL-1 beta elimination impaired the proproliferation effect of NLRP3 hyperexpression. Furthermore, NF-kappa B blockage abrogated IL-1 beta and NLRP3 hyperexpression increased cell growth and invasion. NLRP3 promoted the growth and invasion of gliomas via the IL-1 beta/NF-kappa B p65 signals.