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Glioblastoma is the most aggressive type of brain cancer with a median survival of less than 14 months even after surgery, chemo, and radiotherapy. Immune cells constitute a large proportion of the microenvironment in glioblastoma, sometimes making up almost 60% of all cells. Monocytes, macrophages, dendritic cells, endothelial cells, other innate immune cells, and adaptive immune cells express members of the Nucleotide-binding domain, leucine-rich repeat-containing receptors (NLRs), a family of pattern recognition receptors. NLRs are central to innate immunity, detect danger signals, and form a multi-protein cytosolic complex called the inflammasome. Inflammasomes play a critical role in regulating innate immunity and cancer development. NLRP1 is the first discovered inflammasome sensor member of the NLR family. NLRP1 contains a pyrin domain, 1-6 leucine-rich repeats(LRRs), and a caspase recruitment domain (CARD). The CARD domain can interact with the CARD domain of ASC through homotypic interaction and recruit Caspase-1. Caspase-1 can cleave pro-inflammatory cytokines IL-1β and IL-18, which may regulate cell death. NLRP1 inflammasome activation positively correlates with increased caspase-1 activation and inflammatory response, including elevated IL-1β and IL -18 cytokines in breast cancer cell line (MCF7). Elevated expression of NLRP1 is observed in glioblastoma but the exact role of NLRP1 in glioblastoma remains undiscovered. This research aims to assess the role of NLRP1 in glioblastoma pathophysiology.

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