The APOC3 Knockout HeLa Polyclonal Cells comprise a polyclonal population of HeLa cells that have undergone CRISPR/Cas9-mediated disruption of the APOC3 gene, resulting in loss of apolipoprotein C-III expression. This polyclonal knockout format provides a heterogeneous editing outcome while maintaining the ability to study APOC3 functions in a human epithelial cell context. This product is designed for investigators requiring a reliable, genome-edited cellular model for probing APOC3 biology.
HeLa cells are an immortalized human cervical adenocarcinoma epithelial cell line, originally derived from a cervical cancer biopsy. They are among the most widely used cell lines in biomedical research, valued for their robust proliferation and extensive molecular characterization. HeLa cells have been instrumental in cancer biology and virology, and serve as a versatile host for gene editing. Their epithelial origin offers a distinct platform for investigating lipid metabolism genes within the context of cancer cell physiology.
Apolipoprotein C-III, encoded by APOC3, is a key inhibitor of triglyceride metabolism. It suppresses lipoprotein lipase (LPL)-mediated hydrolysis of triglyceride-rich lipoproteins and blocks hepatic remnant clearance by disrupting APOE interaction with LDL receptor (LDLR) and LDL receptor-related protein 1 (LRP1). APOC3 expression is regulated by HNF4A, PPARA, insulin-responsive FOXO1, and SREBF1. It interacts with APOB, APOE, APOC2, and heparan sulfate proteoglycans. The regulatory network also includes ANGPTL3, ANGPTL4, GPIHBP1, and RXRA, all contributing to lipid homeostasis.
In HeLa cells, APOC3 knockout creates a loss-of-function model to dissect apolipoprotein C-III-dependent effects on lipid handling and metabolic signaling in an epithelial cancer background. This engineered cell line is suited for studying how APOC3 knockout modulates LPL activity, triglyceride accumulation, and remnant uptake without confounding systemic factors. It also enables exploration of APOC3 functions in cancer metabolism and insulin resistance pathways relevant to metabolic syndrome and type 2 diabetes.
Research applications include lipid metabolism studies, hypertriglyceridemia drug screening, cardiovascular disease modeling, and APOC3 interactomics. Compatible techniques include Western blotting, RT-qPCR, LPL activity assays, triglyceride accumulation assays, co-immunoprecipitation, immunofluorescence, Oil Red O staining, flow cytometry, RNA-seq, and reporter gene assays. This polyclonal knockout model supports therapeutic target validation and dissection of apolipoprotein C-III biology. For further information, please contact Ascent Research.
