DPP8 Knockout Huh-7 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the DPP8 gene in the Huh-7 human hepatocellular carcinoma background. This polyclonal loss-of-function model enables the study of DPP8-dependent processes without the constraints of clonal variability, providing a robust tool for investigations into dipeptidyl peptidase 8 biology.
The Huh-7 cell line is derived from the liver tumor of a 57-year-old Japanese male and serves as a well-characterized hepatocellular carcinoma model. These epithelial cells display hepatocyte-like features, including expression of liver-specific markers, and are widely employed to study liver cancer biology, drug metabolism, and hepatic signaling. The Huh-7 background provides a relevant cellular context for examining the roles of DPP8 in hepatic pathophysiology.
DPP8 encodes a cytosolic serine protease that cleaves N-terminal dipeptides from peptide substrates, contributing to immune regulation and apoptosis. In this knockout model, CRISPR/Cas9-mediated disruption of DPP8 removes its inhibitory function on the NLRP1 inflammasome, leading to spontaneous ASC speck formation, caspase-1 activation, and subsequent pyroptotic cell death accompanied by the release of IL-1?? and IL-18. Upstream regulators such as the SP1 transcription factor and NF-??B signaling control DPP8 expression, while downstream targets include the chemokine CXCL10 and collagen-derived peptides. The enzyme interacts with DPP9, SUMO1, and the APC/C complex, positioning DPP8 at a critical node in peptide processing and inflammatory signaling networks.
In the context of hepatocellular carcinoma, DPP8 knockout may reveal key roles in tumor progression and the hepatic immune microenvironment. Loss of DPP8 activity can alter the balance of inflammasome signaling, potentially affecting hepatocyte survival, fibrosis, and anti-tumor immunity. The Huh-7 polyclonal knockout model thus provides a physiologically relevant system to dissect DPP8-mediated regulation of cell cycle and apoptosis in liver cancer cells, and to explore how its disruption impacts chemokine production and inflammasome-driven inflammation.
This knockout product is suited for a range of research applications, including mechanistic studies of NLRP1 inflammasome activation, functional characterization of DPP8 inhibitors, and examination of hepatocellular carcinoma progression. Representative assays include western blotting for NLRP1 and cleaved caspase-1, RT-qPCR for DPP8 mRNA expression, LDH release assays to quantify pyroptosis, IL-1?? ELISA, flow cytometry for active caspase-1 or pyroptotic markers, and DPP8 enzymatic activity measurements. For further details or custom inquiries, please contact Ascent Research.
