The CDKN2C Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from Raji B lymphocytes, carrying a targeted disruption of the CDKN2C gene. This product consists of a heterogeneous pool of cells with loss-of-function at the CDKN2C locus, allowing investigation of p18INK4c tumor suppressor functions in a B-cell lymphoma background without the limitations of monoclonal selection. The polyclonal format is particularly useful for population-based assays where the average effect of gene ablation is assessed, minimizing clonal artifacts.
The Raji parental line is an immortalized B lymphocyte cell line originally established from a Burkitt lymphoma patient. As an EBV-positive lymphoblastoid cell line, Raji cells display characteristics of activated B cells and are widely employed in immunology and cancer research for studies of humoral immunity, antigen presentation, and B-cell malignancies. Their stable growth and well-characterized genetic alterations, including MYC translocation, make them an ideal host for examining the role of cell cycle regulators in lymphomagenesis.
CDKN2C encodes p18INK4c, a cyclin-dependent kinase inhibitor that specifically binds CDK4 and CDK6 in complex with D-type cyclins (Cyclin D1/D2/D3). By inhibiting CDK4/6 kinase activity, p18INK4c prevents the phosphorylation of the retinoblastoma protein RB1. Hypophosphorylated RB1 sequesters E2F1 transcription factor, blocking transcription of S-phase genes and enforcing G1 arrest. TGF-beta signaling via SMAD2/3 transcriptional regulation promotes CDKN2C expression, while MYC transcriptionally represses it. Additionally, B cell receptor signaling and IL-4/STAT6 pathways provide further regulatory inputs, integrating extracellular signals with cell cycle control.
In the Raji cell context, knockout of CDKN2C removes a critical brake on G1/S progression, resulting in unchecked CDK4/6 activity, sustained RB1 hyperphosphorylation, and deregulated E2F1-driven proliferation. This loss-of-function model mimics tumor suppressor inactivation events found in B-cell lymphomas, multiple myeloma, glioblastoma, and melanoma. Combined with endogenous MYC overexpression in Raji cells, this knockout provides a powerful system to dissect the cooperative oncogenic events that drive uncontrolled B-cell expansion and lymphomagenesis.
Researchers can utilize this polyclonal knockout population in diverse experimental workflows, including cell cycle profiling by flow cytometry with propidium iodide staining, assessment of CDK4/6 inhibitor sensitivity using viability assays with palbociclib, and biochemical analysis of the RB pathway via western blotting for phospho-RB1 and p18INK4c. The model is also suited for synthetic lethality screens, co-immunoprecipitation studies of CDK4/6 complexes, and TGF-beta response assays. By averaging across a heterogeneous edited population, this format reduces clonal selection bias in functional studies. For further inquiries, please contact Ascent Research.
