The DPP8 Knockout HGC-27 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of the human DPP8 gene in the HGC-27 gastric carcinoma cell line. This loss-of-function model eliminates DPP8 dipeptidyl peptidase activity while maintaining polyclonality, providing a physiologically relevant system for functional genomics and cancer research.
Derived from a lymph node metastasis of an undifferentiated human gastric carcinoma, HGC-27 cells are a widely characterized model for aggressive gastric cancer. They exhibit rapid proliferation, invasive capacity, and molecular features of epithelial-to-mesenchymal transition, making them suitable for studying tumor progression, metastasis, and therapeutic responses. The undifferentiated phenotype also allows investigation of tumor cell plasticity and interactions with the immune microenvironment.
DPP8 is a serine protease that acts as a dipeptidyl peptidase, cleaving N-terminal dipeptides from substrates with proline or alanine at the penultimate position. It is regulated by upstream signals including NF-??B, AP-1, interferon-gamma, and cellular stress. DPP8 modulates immune cell activation and NF-??B signaling, processes chemokines like IP-10/CXCL10, and influences T cell activation through the TCR-ZAP70-LAT-PLC??1-NFAT pathway. Additionally, DPP8 is implicated in pyroptosis via the NLRP3/ASC/caspase-1 inflammasome, driving IL-1?? secretion and inflammatory cell death, thereby impacting tumor immune surveillance.
In gastric cancer, DPP8 may support immune evasion by trimming bioactive peptides that modulate antitumor immunity. Its knockout in HGC-27 cells is hypothesized to impair this immunomodulatory function, potentially leading to accumulation of unprocessed substrates that trigger NLRP3/caspase-1-dependent pyroptosis. This cell death pathway could directly reduce tumor cell viability and reshape the tumor microenvironment. The model thus permits investigation of the mechanistic links between proteolytic processing, inflammasome activation, and gastric cancer progression, offering a platform for therapeutic target assessment.
The DPP8 Knockout HGC-27 Polyclonal Cells are valuable for gastric cancer research, immunotherapy studies, drug target validation, and inflammation and cell death research. Key assays include western blotting and RT-qPCR for expression analysis, RNA-seq for transcriptomic profiling, LDH release and caspase-1 activation assays for pyroptosis detection, flow cytometry for cell death markers, and migration/invasion assays for metastatic behavior. This robust polyclonal model enables comprehensive functional characterization of DPP8 in relevant cancer contexts. For further information, please contact Ascent Research.
