The MST1R Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population of human Raji B lymphocytes with disrupted MST1R gene expression. This pooled knockout model contains a spectrum of independent edits across the MST1R locus, enabling loss-of-function studies without the clonal selection required for a monoclonal line. The product is designed for robust and flexible investigation of MST1R-dependent biology in a well-characterized B-cell lymphoma context.
Raji cells are an Epstein-Barr virus (EBV)-positive human B lymphocyte cell line derived from a Burkitt lymphoma. They are a widely used model for studying B-cell malignancies, viral oncogenesis, antibody production, and antigen presentation. Raji cells express many B-cell markers and retain functional signaling pathways that are relevant to lymphoma biology and immune cell research, making them an ideal host for targeted gene disruption.
MST1R (RON) is a receptor tyrosine kinase activated by the ligand MST1 (macrophage-stimulating protein). Upon ligand binding, MST1R initiates signaling through the PI3K/AKT, RAS/RAF/MEK/ERK, IKK/NF-??B, and JNK pathways. Downstream targets include AKT, ERK, JUN, NF-??B, STAT3, and ??-catenin, which mediate proliferation, migration, survival, and epithelial-mesenchymal transition. Upstream regulators such as hypoxia and EGF transactivation modulate MST1R activity. The receptor physically interacts with MET, EGFR, ITGB1 (integrin ??1), and SRC, facilitating cross-talk. In this CRISPR-edited polyclonal population, MST1R gene disruption abolishes ligand-induced activation of these cascades, creating a defined loss-of-function context.
In B-cell lymphomas, MST1R signaling may contribute to aberrant proliferation and survival, though its role in lymphoid malignancies is less explored than in solid tumors. The Raji polyclonal knockout model offers a physiologically relevant platform to investigate MST1R function in EBV-driven lymphomagenesis, immune cell transformation, and therapy resistance. This tool is especially valuable for studying the interplay between MST1R and key lymphoma-associated pathways such as NF-??B and PI3K/AKT, and for identifying synthetic lethal interactions or drug sensitivities in B-cell cancers.
This knockout product supports diverse functional assays, including proliferation (MTS), migration (Transwell), and apoptosis (Annexin V) measurements. Phospho-AKT (Ser473) and phospho-ERK (Thr202/Tyr204) detection confirms pathway status, while Sanger sequencing, RT-qPCR, and Western blotting validate knockout. Flow cytometry monitors MST1R surface expression. Applications include mechanistic studies of MST1R oncogenic signaling, drug sensitivity screening for RON-targeted therapies, B-cell lymphoma research, and immune cell functional analysis. For more information, contact Ascent Research.
