CD300LD Knockout 143B Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the CD300LD gene has been disrupted to generate a loss-of-function model in the human osteosarcoma 143B cell line. This product uses a polyclonal knockout strategy, providing a heterogeneous population of cells with targeted gene disruption, suitable for studying CD300LD-dependent functions without the selection of a single clonal isolate. The knockout is achieved via CRISPR/Cas9-mediated gene disruption, enabling researchers to interrogate the role of CD300LD in relevant signaling contexts.
The host cell line, 143B, is a well-characterized subclone of the HOS human osteosarcoma cell line, derived from an osteoblastic osteosarcoma. These cells display high tumorigenic and metastatic potential, making them a robust model for investigating tumor progression, bone-tumor interactions, and metastatic mechanisms. The 143B line retains osteoblastic features and is frequently used in xenograft and orthotopic models to study osteosarcoma biology and evaluate therapeutic interventions.
CD300LD is an activating immune receptor predominantly expressed on myeloid cells. It functions by engaging immunoreceptor tyrosine-based activation motif (ITAM)-containing adaptor proteins, including DAP12 and FcRgamma, which recruit spleen tyrosine kinase (SYK). Activated SYK phosphorylates downstream effectors, leading to activation of the PI3K/AKT pathway, the MAPK cascade (involving MAPK1 and MAPK3), and the NF-??B complex. These signaling events drive the transcriptional upregulation and secretion of pro-inflammatory cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-??). Key upstream regulators include putative ligands and toll-like receptor (TLR) costimulation, while inflammatory cytokines further modulate CD300LD expression and function.
In the 143B osteosarcoma context, CD300LD knockout provides a unique tool to dissect receptor-mediated signaling in tumor cell biology and the interplay with the innate immune system. Although CD300LD is typically associated with myeloid cells, its disruption in osteosarcoma cells allows investigation of potential non-canonical roles or paracrine effects within the tumor microenvironment. This model is particularly valuable for exploring how loss of CD300LD may alter cytokine production, tumor growth, and metastatic behavior in orthotopic and xenograft settings, as well as responses to inflammatory stimuli.
This knockout product is suited for a wide array of research applications, including functional studies of immune receptor signaling, innate immunity modulation, drug target screening, and analysis of osteosarcoma microenvironment interactions. Researchers can employ representative assays such as flow cytometry to assess surface marker expression, quantitative RT-PCR and Western blotting for gene and protein analysis, cytokine secretion assays to measure IL-6 and TNF-?? levels, phospho-kinase profiling to map signaling node activation, and invasion/migration assays to evaluate metastatic potential. The cells are also compatible with co-culture systems to study tumor-immune cell crosstalk and xenograft models for in vivo tumor growth assessment. For additional technical information, please contact Ascent Research.
