The CD300LD Knockout NCI-H1703 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population in which the CD300LD gene has been disrupted to create a loss-of-function model. This product provides a heterogeneous pool of NCI-H1703 lung squamous cell carcinoma cells harboring targeted gene disruption, enabling functional studies of CD300LD in a non-small cell lung cancer background. The knockout is achieved through CRISPR/Cas9-mediated editing without clonal isolation, yielding a representative knockout population suitable for pooled experimental approaches.
The host cell line NCI-H1703 is a widely utilized human lung squamous cell carcinoma line established from a patient with non-small cell lung cancer. It serves as a standard model for investigating EGFR signaling pathways and cancer biology, including tumor cell proliferation, survival, and drug response. The NCI-H1703 line retains key molecular features of squamous cell carcinoma, making it a relevant platform for probing oncogenic mechanisms and therapeutic vulnerabilities.
CD300LD functions as an activating immune receptor that recognizes phosphatidylserine exposed on apoptotic cells. Upon ligand engagement, CD300LD recruits the ITAM-bearing adaptor proteins DAP12 or FcR??, which subsequently activate the spleen tyrosine kinase SYK. This initiates downstream signaling cascades, including PI3K/AKT, MAPK, and NF-??B pathways, culminating in calcium mobilization and the production of pro-inflammatory cytokines such as TNF-?? and IL-6. These pathways collectively regulate efferocytosis and modulate innate immune responses, positioning CD300LD at the intersection of apoptotic cell clearance and inflammatory signaling.
In the context of NCI-H1703 lung carcinoma cells, disruption of CD300LD provides a unique model to dissect its contribution to tumor cell-intrinsic signaling and crosstalk with the microenvironment. Since CD300LD can respond to phosphatidylserine??a ligand often elevated in the tumor milieu due to cell death??its knockout may alter downstream PI3K/AKT and MAPK activity, impacting cell survival, migration, and inflammatory cytokine secretion. This model enables researchers to explore how CD300LD-mediated signaling influences lung cancer cell behavior and immune evasion.
Researchers can employ this CD300LD knockout polyclonal pool in a variety of assays, including Western blotting and RT-qPCR for expression analysis, phospho-signaling analysis to assess pathway activation, and cytokine secretion assays to quantify TNF-?? and IL-6 production. Additional applications include apoptosis assays, migration and invasion studies, and drug sensitivity testing to evaluate the role of CD300LD in therapeutic response. These cells facilitate detailed mechanistic studies of CD300LD-dependent signaling in non-small cell lung cancer and its potential as a therapeutic target. For additional information, please contact Ascent Research.
