The APOE Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the HT29 human colorectal adenocarcinoma cell line. This product comprises a heterogeneous pool of cells carrying targeted disruptions of the APOE gene, resulting in a functional knockout model for studying apolipoprotein E biology. The polyclonal nature of the population better reflects biological diversity and mitigates clonal artifacts.
HT29 cells, the host line, are an adherent, epithelial-like cell line derived from a 44-year-old female with colorectal adenocarcinoma. They serve as a well-established model for intestinal epithelial biology and colorectal cancer research, providing a physiologically relevant platform to investigate lipid metabolism in a tumor context.
APOE encodes apolipoprotein E, a multifunctional glycoprotein central to lipid transport and cholesterol homeostasis. APOE is transcriptionally regulated by LXR (NR1H3), RXR, and PPAR??, and modulated by dietary fatty acids. The protein interacts with LDLR, LRP1, and HSPG to mediate lipoprotein uptake, and facilitates cholesterol efflux via ATP-binding cassette transporters ABCA1 and ABCG1. APOE also participates in reverse cholesterol transport, interacting with APOA1 and LCAT. Additionally, APOE binds ??-amyloid peptide, linking it to Alzheimer’s disease pathology.
In HT29 cells, APOE knockout impairs cholesterol efflux and alters lipid metabolism, which can affect membrane composition and signaling networks. This disruption may influence tumor cell proliferation, migration, and sensitivity to microenvironmental lipids. The model is thus valuable for studying the interplay between lipid homeostasis and colorectal cancer progression. Moreover, the interaction of APOE with receptors such as LDLR and LRP1, which are expressed in HT29 cells, allows for interrogation of ligand-receptor dynamics in a disease-relevant context.
These cells support diverse applications, including lipid metabolism and Alzheimer’s disease studies, cancer biology, and drug screening. Researchers can employ cholesterol efflux assays, lipid uptake experiments, cell viability and migration assays, as well as RT-qPCR and Western blotting to confirm APOE ablation and assess downstream targets like ABCA1 and LDLR. Drug screening campaigns targeting APOE-mediated pathways can benefit from this model to identify compounds that modulate lipid transport or receptor interactions. For additional information, please contact Ascent Research.
