The HLA-E Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human SK-HEP-1 liver adenocarcinoma cell line. This polyclonal population features targeted disruption of the HLA-E gene, eliminating HLA-E protein expression and providing a loss-of-function model for studying immune evasion mechanisms. The polyclonal format captures diverse editing outcomes, offering a robust tool free from single-cell clonality biases.
The parental SK-HEP-1 cell line is an epithelial cell line originally isolated from ascitic fluid of a liver adenocarcinoma patient. It is widely used as a hepatocellular carcinoma (HCC) and metastasis model due to its aggressive tumorigenic properties. SK-HEP-1 cells facilitate investigations of tumor?Cimmune interactions, cell migration, and immune checkpoint regulation in a hepatic cancer context.
HLA-E is a non-classical MHC class I molecule that presents signal-sequence-derived peptides to the inhibitory receptor NKG2A/CD94 on NK cells and CD8+ T cells. This interaction recruits SHP-1 and SHP-2 phosphatases via ITIM motifs, suppressing cytotoxicity. HLA-E expression depends on ??2-microglobulin, TAP, tapasin, and calreticulin, and is transcriptionally regulated by IFN-??, TNF-??, and NF-??B through IRF1 and STAT1. Thus, HLA-E functions as an immune checkpoint, tuning innate and adaptive responses.
In SK-HEP-1 cells, HLA-E knockout removes a key inhibitory axis used by tumors to escape NK cell-mediated lysis and CTL responses. Since SK-HEP-1 is a metastatic HCC model, ablating HLA-E creates a platform for dissecting immune evasion and evaluating immunotherapies. The polyclonal knockout format maintains the heterogeneity of the parental line, avoiding clonal artifacts while ensuring robust gene disruption.
This model supports tumor immunology applications such as NK cell cytotoxicity assays, CD8+ T cell activation studies, and immune checkpoint blockade experiments. Co-cultures with primary immune cells enable analysis of the NKG2A-HLA-E axis. Flow cytometry and immunofluorescence confirm HLA-E loss, while RT-qPCR and Western blotting assess gene and protein levels. Xenograft tumor growth assays evaluate in vivo consequences of HLA-E deletion. For technical details, please contact Ascent Research.
