The CD300LD Knockout UM-UC-3 Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout cell population derived from the UM-UC-3 human bladder urothelial carcinoma line. This product disrupts CD300LD gene expression through targeted genome editing, generating a heterogeneous cell pool suitable for loss-of-function studies. The polyclonal format maintains population diversity, enabling robust phenotypic analysis without clonal bias.
The UM-UC-3 parental line originates from a male patient??s bladder transitional cell carcinoma and is a widely accepted model for malignant urothelial carcinoma. These cells exhibit uncontrolled proliferation, migration, invasion, and apoptosis resistance, reflecting key aggressive cancer properties. They are routinely employed to investigate bladder cancer pathogenesis and therapeutic responses. The CD300LD knockout on this well-characterized background provides a clinically relevant tool for studying tumor biology and immune interactions.
CD300LD encodes a type I transmembrane protein of the CD300 immune receptor family. In myeloid cells, it functions as an activating receptor that, upon ligand binding, couples with the DAP12 adaptor to initiate Syk kinase signaling. This cascade activates the PI3K-Akt and MAPK (ERK and JNK) pathways, ultimately driving NF-??B and AP-1 transcription factors and promoting pro-inflammatory cytokine secretion (e.g., TNF-??, IL-6) and phagocytosis. CD300LD expression is regulated by upstream cytokines such as GM-CSF and IL-4, TLR agonists, and the myeloid transcription factor PU.1. This signaling node integrates immune activation signals central to innate immunity.
Although CD300LD is predominantly studied in immune cells, its ablation in UM-UC-3 bladder cancer cells enables investigation of tumor-intrinsic and microenvironmental roles. Bladder cancers are marked by inflammatory and immune components, and loss of CD300LD facilitates studies of how this receptor contributes to cancer cell behaviors like cytokine release, migration, and phagocytic interaction. Co-culture systems with macrophages or dendritic cells can probe CD300LD-dependent changes in tumor-immune crosstalk, providing insights for immune-based therapeutic strategies in urothelial carcinoma.
Key applications include confirmation of knockout by western blot or RT-qPCR, analysis of downstream phosphorylation events (e.g., phospho-Syk, phospho-Akt), and cytokine profiling via ELISA. Functional assays such as phagocytosis, transwell migration/invasion, and macrophage/dendritic cell co-cultures assess CD300LD??s impact on tumor-immune interactions. These polyclonal cells serve as a platform for target validation in immunomodulatory bladder cancer therapy. For further details, contact Ascent Research.
