The HDLBP Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from HT29 human colorectal adenocarcinoma cells, engineered to disrupt the HDLBP gene. This polyclonal format provides a heterogenous pool of edited cells, enabling functional studies of HDLBP without clone-specific artifacts. The targeted gene disruption eliminates expression of the HDLBP-encoded vigilin protein, a multifunctional RNA-binding protein critical for regulating mRNA stability and translation.
The HT29 host cell line is a widely used model of human colorectal adenocarcinoma, originally isolated from a primary tumor. HT29 cells exhibit characteristics of intestinal epithelial cells, including the ability to differentiate in response to metabolic stimuli. They are frequently employed to investigate colorectal cancer biology, intestinal barrier function, and drug response. The use of HT29 as the parental line provides a physiologically relevant epithelial context for studying HDLBP’s role in cholesterol metabolism and tumor cell behavior.
HDLBP (vigilin) functions downstream of SREBP2 and cellular cholesterol levels, and its expression is additionally regulated by p53. It interacts with apolipoprotein A-I, ribosomes, RNA helicase A, and KHDRBS1 to form complexes that control the fate of target mRNAs. Key downstream targets include c-fos mRNA, which governs cell proliferation, and apolipoprotein B mRNA, central to lipid metabolism. Through these interactions, HDLBP modulates cholesterol efflux and the translational machinery, placing it at the intersection of mRNA stability regulation, cholesterol homeostasis, and colorectal cancer signaling.
In the HT29 colorectal cancer context, HDLBP knockout profoundly impacts cholesterol metabolism and cell growth. Loss of vigilin disrupts the normal coordination between cholesterol sensing and gene expression, potentially impairing cholesterol efflux and altering the expression of proliferation-associated transcripts. This model enables researchers to dissect the contribution of HDLBP to colorectal cancer progression, where dysregulated lipid metabolism and mRNA stability are hallmark features. The polyclonal knockout population is particularly suited for assessing heterogeneous cellular responses without clonal selection bias.
This knockout cell model is ideal for investigating colorectal cancer pathogenesis, lipid metabolism, and RNA biology. Researchers can employ cholesterol efflux assays to quantify functional lipid export, cell proliferation and migration assays to evaluate tumorigenic properties, and RNA immunoprecipitation or RT-qPCR to analyze mRNA binding and expression changes. The cells are also applicable for drug screening studies targeting lipid-related pathways or vigilin interactions. For further information, please contact Ascent Research.
