The MYC Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of Raji B lymphoblastoid cells carrying a targeted disruption of the MYC proto?oncogene. This knockout product is supplied as a versatile polyclonal cell pool, enabling loss?of?function studies without clonal selection artifacts. The gene editing strategy specifically abrogates MYC expression, providing a robust model to dissect the transcription factor??s role in B?cell lymphoma biology.
The Raji parental line derives from a Burkitt lymphoma patient and constitutes a widely used EBV?positive B lymphocyte model. As mature B cells, they retain features of antigen presentation and humoral immune responses while exhibiting hallmark characteristics of aggressive lymphoma, including high proliferative index and resistance to apoptosis. The EBV latency III program expressed in Raji cells contributes to constitutive NF???B and PI3K/AKT pathway activation, creating an oncogenic milieu that cooperates with endogenous MYC dysregulation.
MYC (c?Myc) is a basic helix?loop?helix leucine zipper transcription factor that heterodimerizes with MAX to bind E?box motifs (CACGTG) and regulate genes controlling cell cycle, metabolism, ribosome biogenesis, and apoptosis. Its activity is modulated by interactions with MIZ1, TRRAP, INI1/hSNF5, and histone acetyltransferases GCN5 and TIP60. Upstream pathways including WNT/???catenin (via TCF/LEF), MAPK/ERK (downstream of EGFR/RAS), PI3K/AKT (which stabilizes MYC by inhibiting GSK?3??), STAT3, and NF???B converge on MYC expression and stability. Key transcriptional targets activated by MYC include CCND2, CDK4, E2F factors, TERT, LDHA, and ODC1, while it represses CDKN1A (p21) and CDKN1B (p27). MYC also controls apoptosis by inducing BIM and upregulating BCL2, and cooperates with NOTCH and mTOR/S6K1/EIF4E signaling to enhance protein synthesis.
In Burkitt lymphoma, chromosomal translocations, most commonly t(8;14), place MYC under control of immunoglobulin enhancers, leading to persistent high?level expression that cooperates with EBV latent proteins to drive uncontrolled proliferation and genomic instability. The MYC?knockout Raji model therefore represents a powerful tool to investigate the molecular consequences of acute MYC loss in the context of endemic B?cell lymphoma, allowing researchers to probe oncogene addiction, identify MYC?dependent and ?independent survival pathways, and explore mechanisms of sensitivity or resistance to MYC?targeted strategies, such as BET bromodomain inhibitors.
These polyclonal knockout cells enable transcriptomic (RNA?seq) and epigenomic (ChIP?seq) profiling to map MYC?regulated networks; proliferation, viability, and colony formation assays; flow cytometric cell cycle and apoptosis analyses (Annexin V, caspase activation); metabolic assays using Seahorse or glucose uptake; and drug sensitivity screens with MYC?targeting compounds such as BET inhibitor JQ1. Co?immunoprecipitation studies of MYC?MAX interactions and combinatorial inhibitor studies (PI3K, mTOR, MAPK) are also facilitated. For further information, please contact Ascent Research.
