NLRP3 in human glioma is correlated with increased WHOgrade, and regulates cellular proliferation, apoptosis and metastasis via epithelial-mesenchymal transition and the PTEN/AKT signaling pathway

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