The DPP8 Knockout AGS Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human gastric adenocarcinoma AGS cell line, in which the DPP8 gene has been disrupted to create a loss-of-function model. This pooled polyclonal format provides a heterogeneous mixture of edited cells, enabling robust functional studies without clonal isolation bias. The knockout serves as a versatile tool for investigating DPP8-dependent mechanisms in gastric cancer biology, including chemokine signaling, apoptosis regulation, and tumorigenesis.
The host AGS cell line is a widely used adherent epithelial model originating from a 54-year-old female patient with gastric adenocarcinoma. These cells retain key characteristics of gastric tumor cells, such as dysregulated proliferation and altered signaling networks, making them suitable for studying oncogenic processes and therapeutic responses. The AGS background offers a clinically relevant context for dissecting the role of DPP8 in gastric adenocarcinoma progression, drug sensitivity, and metastatic behavior.
DPP8 encodes a serine protease that specifically cleaves N-terminal dipeptides from substrate proteins, including the chemokines CXCL10, CXCL11, and CXCL12. This enzymatic activity modulates immune cell recruitment and inflammatory signaling by regulating chemokine bioavailability. DPP8 is activated by upstream stimuli such as IFN-?? and TNF-??, and it functions within a signaling network that includes interacting partners like DPP9 and SUMO1. Downstream, DPP8 influences the NF-??B pathway and apoptotic cascades via caspase-3 and Bcl-2 family proteins, thereby connecting protease activity to cell survival and immune response pathways.
Knockout of DPP8 in AGS cells is expected to enhance apoptosis and alter inflammatory signaling, providing a valuable model to elucidate its role in gastric cancer. Loss of DPP8 may impair chemokine processing, leading to reduced CXCL10-mediated signaling and subsequent NF-??B activation, while promoting caspase-3-dependent apoptosis. This model enables the study of how DPP8 deficiency impacts tumor cell proliferation, migration, and immune evasion, with implications for understanding gastric adenocarcinoma pathogenesis and identifying potential therapeutic targets.
Key applications include functional studies of DPP8 in gastric cancer using western blotting, RT-qPCR, and apoptosis assays; screening of DPP8 inhibitors to assess effects on chemokine processing and cell viability; analysis of NF-??B reporter activity and caspase activity; and evaluation of tumor cell migration and drug sensitivity. The cells are suitable for ELISA-based chemokine quantification and flow cytometry to monitor apoptotic markers. Researchers can employ this model to investigate immune modulation in the tumor microenvironment and validate DPP8 as a target in gastric adenocarcinoma. For additional information or custom requests, please contact Ascent Research.
