The ENO2 Knockout Raji Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population in which the human ENO2 gene has been disrupted across a heterogeneous pool of Raji B lymphocytes. This target-gene disruption is achieved via CRISPR/Cas9-mediated gene editing, yielding a population-level loss-of-function model without selection for single-cell clones. The polyclonal format preserves genetic diversity and allows functional interrogation of ENO2 in a context that mirrors the complexity of a native cell population, making it suitable for pooled phenotypic screens and bulk biochemical analyses.
The Raji host cell line is an Epstein?CBarr virus (EBV)-positive B lymphoblastoid cell line originally derived from the maxillary sinus of an 11-year-old African male with Burkitt lymphoma. These suspension-adapted cells are a well-established model for B-cell lymphoma and immunological studies, exhibiting robust proliferation and retaining key features of lymphoid malignancies. The EBV-immortalized background provides a relevant cellular environment for investigating oncogenic signaling, metabolic adaptation, and immune cell biology.
ENO2 (??-enolase) is a glycolytic enzyme that catalyzes the interconversion of 2-phosphoglycerate to phosphoenolpyruvate, a critical step in maintaining glycolytic flux. In Raji cells, ENO2 expression is activated by HIF1A and MYC, linking it to hypoxic signaling and oncogenic metabolic rewiring. Beyond its enzymatic function, ENO2 serves as a cell-surface plasminogen receptor, binding PLG and facilitating its conversion to plasmin by uPA, thereby promoting pericellular proteolysis and cell migration. It also interacts with cytoskeletal proteins (actin, tubulin) and HSP70, integrating metabolic and migratory programs. Downstream, ENO2-generated PEP feeds into pyruvate kinase (PKM2) and lactate dehydrogenase (LDHA), sustaining lactate production and anabolic demands.
In the Raji B-cell lymphoma context, ENO2 knockout disrupts a central node of glycolysis and plasminogen activation, offering a powerful system to dissect the metabolic dependencies of malignant B cells. Given the high glycolytic activity characteristic of Burkitt lymphoma and the role of plasminogen receptors in tumor invasion, this model enables direct assessment of ENO2??s contribution to proliferation, survival, and motility. The polyclonal knockout approach avoids clonal artifacts and reveals population-level vulnerabilities, making it especially useful for studying heterogeneous responses to metabolic inhibition or anti-migratory therapies.
Researchers can employ the ENO2 Knockout Raji Polyclonal Cells for diverse applications, including the investigation of metabolic reprogramming in B-cell lymphoma, functional studies of ENO2 in cancer cell proliferation and survival, and target validation for anti-glycolytic therapies. Typical assays include Western blotting for ENO2, RT-qPCR to confirm gene disruption, Seahorse glycolysis stress tests, lactate production measurements, plasminogen binding ELISA, Transwell migration assays, and flow cytometry for cell surface enolase. These cells also serve as a valuable tool for plasminogen-dependent cell migration and invasion assays, and for screening compounds that target glycolytic or plasminogen receptor functions. For further information or to discuss custom modifications, please contact Ascent Research.
