GSDMD Knockout HCT 116 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the human GSDMD gene in the HCT 116 colorectal carcinoma epithelial cell line. This product consists of a heterogeneous pool of HCT 116 cells with targeted disruption of GSDMD, providing a robust loss-of-function model for investigating gasdermin D-dependent processes while minimizing clonal selection artifacts.
The parental HCT 116 cell line is a well-characterized colorectal carcinoma model derived from a male patient. It harbors oncogenic KRAS G13D and ??-catenin mutations and displays microsatellite instability, creating a clinically relevant genetic background for studying inflammation-linked tumorigenesis, epithelial innate immunity, and cancer cell death.
GSDMD acts as the principal executioner of pyroptosis, a pro?inflammatory programmed cell death. Canonical inflammasomes, such as those containing NLRP3, AIM2, NLRC4, or Pyrin, nucleate the adaptor ASC (PYCARD) and recruit pro?caspase?1, while non?canonical activation involves caspase?4 and caspase?5. These caspases cleave GSDMD, releasing the N?terminal pore?forming domain that oligomerizes in the plasma membrane. The resulting pores disrupt ionic homeostasis, leading to cell swelling, lysis, and passive release of mature IL?1??, IL?18, HMGB1, and LDH. GSDMD function is further regulated by interactions with NEK7 and binding to membrane phospholipids such as cardiolipin and phosphatidylinositol phosphates.
In the HCT 116 colorectal cancer background, GSDMD knockout offers a precise tool to dissect the role of pyroptosis in tumor biology. The presence of KRAS G13D and ???catenin mutations may alter inflammasome responsiveness and downstream cytokine secretion, enabling researchers to explore how oncogenic pathways intersect with inflammatory cell death. This model is valuable for studying pyroptosis?mediated effects on tumor cell survival, immune evasion, and the response to chemotherapeutic agents.
Researchers can employ this polyclonal knockout cell population for a broad range of applications, including detailed mechanistic studies of inflammasome signaling, screening of small?molecule inhibitors targeting NLRP3 or caspase?1, and investigation of host?pathogen interactions. Standard assays such as Western blotting for GSDMD cleavage, LDH release measurement, IL?1?? ELISA, flow cytometry for propidium iodide uptake, and immunofluorescence for GSDMD subcellular localization are fully compatible. Inflammasome stimulation with ATP, nigericin, or lipopolysaccharide allows controlled activation, while quantitative RT?PCR and RNA?sequencing provide transcriptional readouts. For additional technical specifications and ordering information, please contact Ascent Research.
