The CD300LD Knockout Ca Ski Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human cervical carcinoma epithelial cell line Ca Ski. This gene-disrupted model targets CD300LD (CLM-1), enabling loss-of-function studies in epithelial contexts. The polyclonal format captures diverse editing events, supporting robust investigation of CD300LD biology without clonal bias.
Ca Ski is a metastatic cervical carcinoma cell line with integrated HPV-16 genome, serving as a key model for HPV-driven oncogenesis. These adherent epithelial cells retain squamous carcinoma features and express E6/E7 oncoproteins, facilitating research on viral-host interplay and tumor progression.
CD300LD is an immunoreceptor tyrosine-based activation motif (ITAM)-coupled receptor that signals via the DAP12 adaptor protein. Upon ligand engagement, such as phosphatidylserine, DAP12 becomes phosphorylated, recruiting SYK kinase which subsequently activates PLC?? and PI3K-dependent pathways. This cascade leads to NF-??B and MAPK phosphorylation, culminating in enhanced phagocytic activity and secretion of pro-inflammatory cytokines like TNF-?? and IL-6. CD300LD expression is driven by the transcription factors NF-??B and PU.1, and can be upregulated by TLR agonists (e.g., LPS) and cytokines such as TNF-?? and IL-1??. Negative regulation is exerted by SHP-1/SHP-2 phosphatases that dephosphorylate DAP12, attenuating signaling. While best characterized in myeloid cells, CD300LD expression in epithelial cancers may influence inflammatory responses and tumor-immune dynamics.
In the Ca Ski cell model, CD300LD knockout disrupts potential tumor-intrinsic immune signaling, enabling dissection of how this receptor impacts epithelial cell cytokine networks, proliferation, and migration. The HPV-16-positive background permits investigation of viral oncoprotein interactions with CD300LD-mediated pathways. This system provides a platform for studying the contribution of CD300LD to immune evasion and pro-tumorigenic inflammation in cervical cancer, and for evaluating its role in the tumor microenvironment.
This polyclonal knockout population is compatible with standard assays: western blotting for CD300LD and downstream targets (SYK, NF-??B); RT-qPCR for transcriptional changes; flow cytometry for surface marker analysis; ELISA for secretome profiling; phagocytosis assays to measure engulfment activity; co-culture with immune cells to assess tumor-immune interactions; and RNA-seq for transcriptome-wide impacts. It serves as a powerful model for cervical cancer immunology, immune checkpoint regulation studies, and drug screening for immunomodulators. For further technical inquiries, please contact Ascent Research.
