ELANE Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the HGC-27 human gastric carcinoma epithelial cell line, harboring targeted disruption of the ELANE gene. This product serves as a loss-of-function model to study the roles of neutrophil elastase in gastric cancer biology, inflammation, and programmed cell death. The polyclonal format provides a heterogeneous mixture of edited genotypes, suitable for functional studies where average phenotypic effects are assessed without clonal selection.
The HGC-27 cell line was derived from a lymph node metastasis of gastric adenocarcinoma and exhibits typical epithelial morphology. It is extensively used as a model for gastric cancer research, including studies on tumor progression, metastatic dissemination, and drug screening. Its metastatic origin makes it particularly relevant for examining protease-driven invasion and interactions with the tumor microenvironment.
ELANE encodes neutrophil elastase, a serine protease stored in neutrophil azurophil granules and released during degranulation. It degrades extracellular matrix proteins (e.g., elastin, fibronectin, collagen) and cleaves substrates such as gasdermin D (GSDMD) and E-cadherin (CDH1), promoting pyroptosis and invasion, respectively. Its expression is regulated by transcription factors including PU.1, CEBPA, and MYB, and its activity is controlled by inhibitors like SERPINA1, SLPI, and elafin. Activation of PAR-2 (F2RL1) by elastase couples to MAPK/ERK, PI3K-Akt, and NF-??B pathways. Thus, ELANE knockout eliminates a central proteolytic hub linking extracellular matrix remodeling, inflammation, and cell death.
In the HGC-27 background, ELANE knockout is expected to reduce cleavage of GSDMD and CDH1, attenuating pyroptotic cell death and invasive capacity. As the cell line originates from a metastatic site, this model enables dissection of how neutrophil elastase contributes to gastric cancer metastasis and stromal remodeling. It also allows examination of compensatory mechanisms and interactions with endogenous inhibitors in a clean genetic context.
Key applications include investigating ELANE-dependent migration and invasion (using Boyden chamber assays), probing gasdermin D-mediated pyroptosis via propidium iodide uptake and cleavage analyses, screening elastase inhibitors, and modeling neutropenia-associated phenotypes. Compatible readouts include Western blotting, RT-qPCR, ELISA for IL-1??, elastase activity assays, and viability measurements. For further assistance, contact Ascent Research.
