The GSDMD Knockout T-47D Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the T-47D human breast carcinoma epithelial line, with targeted disruption of the GSDMD gene. This heterogeneous loss-of-function model enables study of GSDMD-dependent processes in an estrogen receptor-positive (ER+) breast cancer context. The knockout was generated using CRISPR/Cas9-mediated gene disruption, resulting in stable ablation of functional GSDMD protein across the population.
The parental T-47D cell line originates from pleural effusion of a ductal carcinoma, serving as a widely used ER+ breast cancer model. It retains estrogen receptor ?? expression and key signaling pathways of hormone-responsive breast cancer, making it suitable for investigating intersections between inflammatory cell death and hormone-driven tumor biology.
GSDMD encodes the pore-forming executor of pyroptosis, an inflammatory cell death pathway. Inflammasome sensors (NLRP3, NLRC4, AIM2, pyrin) activate inflammatory caspases (caspase-1, -4, -5) that cleave GSDMD, releasing the N-terminal domain to oligomerize and form membrane pores. This results in plasma membrane rupture, cytokine release (IL-1??, IL-18), and pyroptotic cell death. Key pathway components include ASC, NLRP3, and caspase-1, which together with GSDMD constitute a core inflammasome signaling module.
In T-47D cells, GSDMD knockout permits dissection of pyroptosis in ER+ breast cancer, such as effects on tumor cell viability, inflammatory cytokine profiles, and responses to therapeutics. Because pyroptosis can modulate tumor immune microenvironments, this model is valuable for exploring how GSDMD-mediated cytokine secretion influences cancer inflammation. It also allows assessment of GSDMD??s role in drug-induced immunogenic cell death.
Typical applications include pyroptosis mechanism studies, inflammasome activation assays (e.g., LPS/ATP or nigericin stimulation), and screening for pyroptosis inhibitors. Representative assays comprise western blot for GSDMD cleavage, LDH release measurement, IL-1?? ELISA, caspase-1 activity assays, and immunofluorescence detection of N-terminal GSDMD pore formation. For additional technical information, please contact Ascent Research.
