MCC Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji B lymphocyte line, featuring targeted disruption of the MCC tumor suppressor gene. This polyclonal pool provides a loss-of-function model for investigating MCC-dependent regulatory mechanisms without clonal isolation, retaining genetic heterogeneity typical of polyclonal knockout backgrounds.
The parental Raji cell line is an EBV-positive human B lymphoblastoid line originating from a Burkitt lymphoma, characterized by constitutive NF-??B activity and suspension growth. These cells are widely used as a model for B-cell biology, antigen presentation, antibody production, and immune regulation, and they serve as a relevant platform for studying lymphomagenesis and lymphoblastoid cell signaling.
MCC encodes a coiled-coil protein that acts as a negative regulator of the Wnt/??-catenin signaling pathway. It directly interacts with ??-catenin and components of the destruction complex, including APC, AXIN1, and AXIN2, to promote ??-catenin phosphorylation by GSK3??, thereby tagging ??-catenin for ubiquitin-dependent proteasomal degradation. Consequently, MCC represses the transcription of Wnt target genes such as MYC and CCND1, which are activated by TCF/LEF transcription factors. Upstream Wnt ligands (e.g., Wnt3a) bind Frizzled/LRP5/6 receptors, leading to DVL-mediated disassembly of the destruction complex and stabilization of ??-catenin. MCC functions as a critical molecular brake in this pathway, and its disruption removes a key constraint on pathway output.
In Raji B cells, where NF-??B signaling and lymphomagenic potential are already elevated, MCC knockout further deregulates Wnt/??-catenin activity, potentially enhancing proliferation, inhibiting apoptosis, and amplifying oncogenic transcriptional programs. This makes the polyclonal MCC knockout Raji cells a physiologically relevant model for dissecting the interplay between NF-??B and Wnt pathways in B-cell lymphomas and for evaluating the contribution of MCC loss to malignant transformation.
These polyclonal knockout cells enable a variety of experimental applications to study tumor suppressor mechanisms and Wnt signaling dysregulation. Representative assays include Western blotting for ??-catenin stability, TCF/LEF luciferase reporter assays to measure transcriptional output, RT-qPCR for MYC and CCND1 expression, and functional readouts such as cell viability, Annexin V apoptosis, and cell cycle flow cytometry. Co-immunoprecipitation can probe interactions with ??-catenin and destruction complex members. The cells are also suitable for screening Wnt-modulating compounds and performing functional genomics studies in B-cell cancer contexts. For further information on custom knockout services, please contact Ascent Research.
