B2M Knockout KYSE-30 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the KYSE-30 human esophageal squamous cell carcinoma cell line, with targeted disruption of the B2M gene encoding beta-2-microglobulin. This loss-of-function model is provided as a polyclonal mixture, enabling researchers to study the collective effect of B2M disruption without the constraints of clonal selection.
KYSE-30 is a well-characterized human esophageal squamous cell carcinoma cell line, serving as a model for esophageal epithelial cell biology and carcinoma. It retains key epithelial features and tumorigenic properties, making it suitable for studying cancer progression, drug response, and immune interactions in the context of esophageal cancer.
Beta-2-microglobulin is an essential component of MHC class I molecules, forming a stable complex with the heavy chains (HLA-A, B, C) to present peptide antigens. B2M expression is upregulated by interferons (IFN-??, IFN-??) through transcription factors IRF1 and NF-??B. In the antigen presentation pathway, B2M interacts with the peptide-loading complex including TAP1/TAP2, tapasin, calreticulin, and ERp57, ensuring proper MHC class I assembly and surface expression. Disruption of B2M therefore results in reduced MHC class I surface expression, impairing CD8+ T cell recognition and promoting tumor immune evasion.
In the KYSE-30 cell line, B2M knockout models the immune evasion mechanisms often observed in tumors that downregulate MHC class I to escape immunosurveillance. This polyclonal population recapitulates heterogeneous B2M loss, mirroring in vivo tumor heterogeneity. It is particularly relevant for esophageal squamous cell carcinoma, where immune checkpoint inhibitors are being explored. The knockout allows investigation of how loss of antigen presentation affects tumor growth and response to immunotherapies.
This product is suited for immune checkpoint inhibitor response studies, tumor immunogenicity assessment, and MHC class I deficiency modeling. Representative assays include flow cytometry for MHC class I surface expression, T cell killing assays, IFN-?? treatment to measure MHC class I upregulation, RT-qPCR for HLA class I genes, western blotting for B2M and heavy chain, co-culture with antigen-specific T cells, and tumor xenograft growth in immunocompromised versus humanized mice. For further details and ordering information, please contact Ascent Research.
