The LZTFL1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9?edited polyclonal knockout population in which the LZTFL1 tumor suppressor gene has been disrupted in the Raji B lymphocyte line. This polyclonal model provides a pool of edited cells that collectively lack functional LZTFL1 protein, offering a physiologically relevant system for studying gene loss without the biases inherent to single?cell clones. The population?level editing ensures sufficient heterogeneity for robust functional genomics, drug screening, and signaling studies.
The Raji cell line, derived from an 11?year?old African male with Burkitt??s lymphoma, is Epstein?Barr virus (EBV)?Cpositive and widely used as a model for B?cell lymphomagenesis and viral oncogenesis. It displays constitutive NF???B activity and expresses viral latency genes that create a unique context for examining tumor suppressor gene function. This background allows investigation of how LZTFL1 deletion interacts with EBV?driven pathways to influence immune signaling, proliferation, and transformation.
LZTFL1 localizes to the cytoplasm and primary cilium, where it facilitates BBSome complex assembly and ciliary transport. It acts upstream of E?cadherin and ???catenin stabilization while repressing vimentin and N?cadherin during EMT. Upstream regulators include TGF??? and inflammatory cytokines; downstream targets encompass Gli1 and the chemokine receptor CCR5. By interacting with BBS9, Smad4, and ???catenin, LZTFL1 integrates ciliary and adhesion signaling with immune modulation, and its knockout consequently disrupts ciliogenesis, enhances Hedgehog pathway activation, and promotes mesenchymal marker expression.
In Raji cells, which lack primary cilia, LZTFL1 knockout reveals cilia?independent tumor suppressor roles. The model permits dissection of LZTFL1??s influence on EMT?like processes in B?cell lymphoma and its impact on Hedgehog signaling without confounding ciliogenesis effects. Moreover, the EBV?positive background may expose synergistic oncogenic interactions between LZTFL1 loss and viral latency programs, potentially altering CCR5?mediated chemokine responses that shape tumor microenvironment interactions.
Applications include mechanistic studies of LZTFL1 in B?cell lymphomagenesis, COVID?19 host factor research, and EMT characterization in hematopoietic malignancies. Assays such as Western blotting for E?cadherin and vimentin, RT?qPCR for Gli1 and CCR5, flow cytometry for CD19 and CCR5, transwell migration, and co?immunoprecipitation of BBSome components are readily performed with this polyclonal population. Transcriptomic profiling and drug sensitivity screening against Smoothened inhibitors further exploit the model??s versatility. For additional details, please contact Ascent Research.
