Glioma is the most prevalent and fatal primary
tumor of the central nervous system in adults, while the development of effective therapeutic strategies in clinical practice remain a challenge.
Nucleotide-binding domain
leucine-rich family
pyrin-containing 3 (NLRP3) has been reported to be associated with
tumorigenesis and progression; however, its expression and function in human
glioma remain unclear. The present study was designed to explore the biological role and potential mechanism of NLRP3 in human
glioma. The results demonstrated that overexpression of NLRP3, apoptosis-associated speck-like
protein containing a caspase-recruitment domain (ASC), caspase‑1 and
interleukin (IL)‑1β
protein in human
glioma tissues were significantly correlated with higher World Health Organization grades. The in vitro biological experiments demonstrated that NLRP3 downregulation significantly inhibited the proliferation, migration and invasion, and promoted the apoptosis of SHG44 and A172
glioma cell lines. Furthermore, western blot assays revealed that the downregulation of NLRP3 significantly reduced the expression of ASC, caspase‑1 and IL‑1β
protein. Furthermore, NLRP3 knockdown caused the inhibition of epithelial-mesenchymal transition (EMT), and inhibited the phosphorylation of AKT
serine/threonine kinase (AKT) and phosphorylation of
phosphatase and
tensin homolog (PTEN). Consistently, the upregulation of NLRP3 significantly increased the expression of ASC, caspase‑1, IL‑1β and phosphorylated-PTEN, promoted proliferation, migration, invasion and EMT, inhibited apoptosis, and activated the AKT signaling pathway. The data of the present study indicate that NLRP3 affects human
glioma progression and
metastasis through multiple pathways, including EMT and PTEN/AKT signaling pathway regulation, enhanced
inflammasome activation, and undefined
inflammasome-independent mechanisms. Understanding the biological effects of NLRP3 in human
glioma and the underlying mechanisms may offer novel insights for the development of
glioma clinical therapeutic strategies.