The HDLBP Knockout SK-HEP-1 Polyclonal Cells product constitutes a CRISPR/Cas9-edited polyclonal cell population engineered to disrupt the HDLBP gene (encoding vigilin) in the SK-HEP-1 host background. These knockout cells provide a loss-of-function model that eliminates vigilin protein expression, enabling systematic investigation of its roles in RNA metabolism and lipid homeostasis. The polyclonal nature ensures representation of diverse editing outcomes while maintaining bulk functional ablation, making this product suitable for assays requiring pooled populations rather than single-cell-derived clones.
The host cell line SK-HEP-1 is a human epithelial cell line derived from the ascites of a patient with liver adenocarcinoma. It is widely utilized as a model for hepatocellular carcinoma (HCC) research, exhibiting characteristic features of hepatic malignancy. SK-HEP-1 cells endogenously express components of the cholesterol metabolic machinery and are capable of HDL binding and cholesterol efflux, rendering them a relevant system to dissect vigilin-dependent lipid transport processes in a cancer context.
Vigilin is a multifunctional RNA-binding protein post-transcriptionally regulating mRNAs central to lipid metabolism. It directly interacts with high-density lipoprotein (HDL) and its major apolipoproteins APOA1 and APOB, bridging lipoproteins to ribosomal subunits and target transcripts. Transcriptionally regulated by SREBP1, SREBP2, and PPARG, vigilin controls the stability and translation of APOB, APOE, and LDLR mRNAs, modulating production of proteins for lipoprotein assembly and cholesterol clearance. Thus, vigilin is pivotal in HDL-mediated cholesterol efflux, cooperating with ABCA1 and LCAT to sustain cholesterol homeostasis.
Ablation of HDLBP in SK-HEP-1 cells disrupts this regulatory circuit, leading to impaired HDL-mediated cholesterol efflux and altered lipid homeostasis. The resulting phenotype likely compromises the cell??s ability to manage intracellular cholesterol levels, which may influence proliferation, migration, and other malignant traits associated with hepatocellular carcinoma. This knockout model therefore provides a phenotypically relevant platform to explore how vigilin integrates RNA regulation with lipid metabolism in liver cancer biology, facilitating studies on hypercholesterolemia, atherosclerosis, and tumor progression.
Researchers can employ this product in a range of applications including cholesterol efflux assays, HDL binding experiments, RNA immunoprecipitation (RIP), Western blotting, RT-qPCR, and cell proliferation or migration/invasion studies. Transcriptome-wide analyses via RNA-seq can further delineate vigilin-dependent expression changes. These polyclonal knockout cells are especially suited for functional rescue experiments, signaling pathway dissection, and drug screening efforts aimed at targeting lipid metabolism in cancer. For ordering, technical support, or custom inquiries, please contact Ascent Research.
