The CASP4 Knockout HGC-27 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout population originating from the HGC-27 human gastric adenocarcinoma cell line, in which the endogenous CASP4 gene has been disrupted. This polyclonal format provides a heterogeneous loss-of-function model free from clonal selection artifacts, ensuring reliable performance in population-averaged assays. The stable gene disruption is achieved through CRISPR/Cas9-mediated genome editing, generating a versatile research tool for studying CASP4-dependent processes.
The parental HGC-27 cell line is a poorly differentiated epithelial gastric adenocarcinoma culture originally established from a lymph node metastasis. It serves as a widely used model for investigating gastric cancer biology, including mechanisms of invasion, metastatic dissemination, and inflammatory signaling within the tumor microenvironment. Its metastatic lineage offers particular utility for studies on aggressive cancer phenotypes.
CASP4 encodes a cytosolic receptor for bacterial lipopolysaccharide (LPS). Upon LPS engagement, CASP4 undergoes CARD domain-mediated oligomerization, leading to activation and subsequent proteolytic processing of gasdermin D (GSDMD). Cleaved GSDMD forms membrane pores that trigger pyroptosis and enable release of mature IL-1?? and IL-18. CASP4 expression is primed by Toll-like receptor 4 (TLR4) and type I interferon signaling, and it functions within the non-canonical inflammasome pathway alongside NLRP3 to orchestrate inflammatory host defenses.
Knockout of CASP4 in HGC-27 cells enables dissection of intracellular LPS sensing in the context of gastric cancer, where exposure to bacterial products??such as those from Helicobacter pylori??can modulate tumor-associated inflammation and cancer cell fate. Researchers can investigate how loss of CASP4 impacts pyroptotic cell death, cytokine secretion, and crosstalk with other innate immune pathways, providing insights relevant to gastric cancer progression, sepsis, and inflammatory bowel disease.
Typical applications include western blotting to assess cleavage of CASP4 and GSDMD, RT-qPCR for IL-1?? and IL-18 transcripts, LDH release assays for pyroptosis quantification, and flow cytometry to monitor cell death. Co-immunoprecipitation can probe direct LPS?CCASP4 binding. This product supports research in innate immunity, pyroptosis, gastric inflammation, and infectious disease. For additional technical information, contact Ascent Research.
