The MTDH Knockout Raji Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the human MTDH (metadherin) gene in the Raji B lymphocyte line. This loss-of-function model is produced via CRISPR/Cas9-mediated gene disruption, yielding a heterogeneous pool of cells with targeted MTDH ablation, enabling functional studies of MTDH-dependent signaling without clonal selection biases.
The Raji host cell line is an Epstein-Barr virus (EBV)-positive Burkitt??s lymphoma-derived B lymphocyte model widely employed in cancer biology and immunology research. Characterized by its lymphoblastoid morphology and rapid proliferation, Raji cells retain key features of B-cell malignancies, including constitutive NF-??B signaling driven by the viral oncoprotein LMP1, making them a relevant system for dissecting oncogenic pathways and EBV?Chost interactions.
MTDH encodes a multifunctional scaffold protein that integrates multiple oncogenic signals. It physically interacts with NF-??B p65, I??B??, PI3K, AKT, ??-catenin, SND1, and CBP/p300 to coordinate transcriptional and signaling complexes. MTDH facilitates PI3K/AKT phosphorylation cascades and promotes ??-catenin nuclear translocation, thereby activating pro-proliferative and anti-apoptotic gene networks. Upstream regulators such as c-Myc, NF-??B, Ha-ras, and the EBV LMP1 protein converge on MTDH to amplify downstream effectors including MMP-9 and NF-??B target genes.
In the Raji cellular context, MTDH knockout disrupts scaffold-mediated NF-??B and PI3K/AKT activation, impairing pro-survival signals and sensitizing cells to apoptosis. Loss of MTDH also attenuates ??-catenin-dependent transcription, diminishing oncogenic proliferation and invasion potential. This model is particularly valuable for investigating how EBV-driven LMP1 signals exploit MTDH to sustain malignant phenotypes, and for exploring how MTDH contributes to chemoresistance mechanisms in B-cell lymphomas.
Typical applications include functional genomics of MTDH in lymphoma, chemoresistance mechanism studies, drug target validation, and EBV?Chost interaction research. Researchers can employ a suite of representative assays such as Western blotting, RT-qPCR, cell proliferation and apoptosis assays, colony formation, Transwell migration, NF-??B luciferase reporter assays, co-immunoprecipitation, and drug sensitivity testing to dissect MTDH signaling networks. For further information and technical support, please contact Ascent Research.
