The B2M Knockout MCF-7 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human MCF-7 breast adenocarcinoma cell line, featuring targeted disruption of the beta-2-microglobulin (B2M) gene. This polyclonal product contains a heterogeneous mix of edited cells, each carrying distinct gene-disrupting events at the B2M locus, collectively abolishing B2M protein expression across the population.
The parental MCF-7 cell line is an estrogen receptor-positive (ER+), progesterone receptor-positive (PR+) luminal A subtype breast adenocarcinoma model, originally isolated from the pleural effusion of a metastatic patient. These adherent epithelial cells retain key features of hormone-responsive breast cancer, including dependence on estrogen for proliferation and expression of luminal markers, making them a widely used system for studying hormone receptor-positive breast cancer biology and therapeutic response.
Beta-2-microglobulin (B2M) is the invariant light chain of major histocompatibility complex (MHC) class I molecules, forming a stable complex with the heavy chains (HLA-A, B, and C) and interacting with the peptide-loading complex components including tapasin, calreticulin, and ERp57 to facilitate antigen presentation on the cell surface. B2M expression is transcriptionally regulated by interferons, particularly IFNG, through IRF1 and NF-??B signaling, and is induced by pro-inflammatory cytokines such as TNF-alpha and IL-2. Upon peptide loading, the fully assembled MHC class I complex presents intracellular antigens to the T cell receptor on CD8+ cytotoxic T lymphocytes, enabling immune surveillance and elimination of aberrant cells. Disruption of B2M abrogates this antigen presentation pathway, impairing CD8+ T cell recognition and promoting immune evasion.
In the context of MCF-7 breast cancer cells, loss of B2M mimics a clinically relevant mechanism of immune escape observed in various malignancies, including breast carcinomas. By eliminating surface MHC class I expression, these knockout cells provide a defined model to study how hormone receptor-positive tumors evade cytotoxic T cell responses. This system allows dissection of the interplay between endocrine signaling pathways and immune recognition, and can be used to investigate compensatory immune evasion strategies that arise upon antigen presentation deficiency.
These B2M knockout MCF-7 polyclonal cells are suited for a variety of immuno-oncology applications, including cytotoxicity assays to evaluate CD8+ T cell-mediated killing, flow cytometry and immunofluorescence to confirm loss of MHC class I surface expression, and transcriptomic profiling via RNA-seq to uncover transcriptional adaptations. They can be used to identify neoantigen presentation dependencies, screen for immune checkpoint inhibitors that bypass MHC class I loss, or generate antigen-loss variant models for elucidating resistance to T cell-based therapies. For additional information or customized services, please contact Ascent Research.
