The GSDME Knockout CAL-27 Polyclonal Cells are a CRISPR/Cas9-edited human polyclonal knockout cell population in which the GSDME gene has been disrupted, providing a loss-of-function model for studying gasdermin E (GSDME)-mediated pyroptosis and inflammatory signaling. This polyclonal pool, derived from the CAL-27 oral squamous cell carcinoma line, enables robust population-level analysis of GSDME-dependent phenotypes without clonal selection bias. It is suitable for high-throughput screening and mechanistic studies investigating chemotherapeutic responses and immunogenic cell death.
CAL-27 is an adherent epithelial cell line established from a human tongue squamous cell carcinoma. It carries a p53 mutation and is HPV-negative, representing a common genetic profile in head and neck cancers. Widely used in cancer biology, CAL-27 serves as a clinically relevant host for dissecting oral tumorigenesis, drug resistance, and cell death pathways.
GSDME encodes the pyroptosis executioner gasdermin E. Upon cleavage by caspase-3 or granzyme B, its N-terminal fragment forms plasma membrane pores, triggering cell lysis and release of pro-inflammatory mediators such as IL-1??, IL-18, and HMGB1, as well as LDH. GSDME activation lies downstream of mitochondrial apoptotic signaling: cytochrome c release promotes caspase-9 activation via APAF1, leading to caspase-3 cleavage. BAX and BAK facilitate mitochondrial permeabilization. GSDME also interacts with cardiolipin and phosphatidylinositol phosphates for membrane targeting. Its expression is regulated by DNA methylation and TP53, and silencing in cancers contributes to chemoresistance.
In oral squamous cell carcinoma, GSDME is often epigenetically silenced, and its re-expression can switch apoptosis to immunogenic pyroptosis. The GSDME Knockout CAL-27 Polyclonal Cells therefore provide a critical platform to investigate how loss of GSDME impacts chemotherapy sensitivity and tumor immune evasion. The p53-mutated background also enables studies of p53-independent regulatory mechanisms controlling pyroptosis.
Key applications include Western blotting for GSDME cleavage, LDH release and propidium iodide uptake assays, IL-1?? ELISA, caspase-3 activity measurements, confocal microscopy of pore formation, and chemotherapy sensitivity testing (CCK-8). The cells are also valuable for colony formation assays, co-culture systems assessing inflammation, and drug screening for pyroptosis inducers. For further details, please contact Ascent Research.
