The APOC3 Knockout HT29 Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal population derived from the HT29 human colorectal adenocarcinoma cell line, designed to disrupt the APOC3 gene. This heterogeneous knockout model preserves the parental line??s epithelial characteristics while abolishing APOC3 expression, making it suitable for investigating gene function in a pooled-cell format without clonal isolation.
HT29 cells originate from a human colorectal adenocarcinoma and serve as a widely used epithelial model for studying intestinal cell biology, colorectal cancer, and absorptive processes. These adherent cells retain the ability to express certain apolipoproteins and lipid-handling pathways, providing a relevant intestinal platform for examining APOC3??s role in lipid metabolism.
APOC3 encodes apolipoprotein C-III, a potent inhibitor of lipoprotein lipase (LPL) and hepatic lipase. By impairing the hydrolysis of triglycerides in very-low-density lipoproteins (VLDL) and chylomicrons, APOC3 delays the clearance of triglyceride-rich remnant particles from the circulation, contributing to hypertriglyceridemia. Its expression is regulated by insulin (via FoxO1), glucose (through ChREBP), SREBP-1c, PPAR??, LXR, TNF??, and retinoic acid. Downstream, APOC3 interacts with ApoB and ApoE, and it interferes with the binding of ApoE to receptors such as the LDL receptor-related protein and VLDL receptor, thereby reducing hepatic remnant uptake.
In the HT29 intestinal epithelial context, APOC3 knockout allows researchers to dissect cell-autonomous lipid metabolism pathways. HT29 cells can be stimulated to secrete chylomicron-like particles, and deletion of APOC3 is expected to enhance LPL-mediated triglyceride hydrolysis and facilitate receptor-mediated particle clearance. This model is therefore highly relevant for dissecting the cellular drivers of hypertriglyceridemia, cardiovascular risk, metabolic syndrome, and non-alcoholic fatty liver disease, and for testing interventions that target APOC3.
These cells support a broad panel of assays including Western blotting and RT-qPCR for APOC3 and related genes, LPL activity and triglyceride secretion measurements, lipoprotein binding experiments, oil red O staining for lipid accumulation, and ELISA-based quantification of ApoB and triglycerides. They are also amenable to fatty acid oxidation analyses. The knockout model is valuable for drug screening of lipid-lowering agents and for exploring APOC3-mediated signaling in intestinal epithelium. For additional details, please contact Ascent Research.
