The CD300LD Knockout HGC-27 Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of the CD300LD gene in the HGC-27 human gastric carcinoma cell line. This loss-of-function model is generated through CRISPR/Cas9-mediated gene targeting, yielding a heterogeneous knockout pool that avoids single-cell clonal selection and maintains population-level genetic diversity. The polyclonal format is advantageous for studies requiring robust, reproducible phenotypes across a mixed cell population.
The HGC-27 host cell line is an epithelial tumor model derived from the metastatic lymph node of a poorly differentiated gastric adenocarcinoma in a human male. These adherent cells retain aggressive growth characteristics and invasive properties, recapitulating key aspects of gastric cancer biology. As a widely used gastric carcinoma cell line, HGC-27 provides a clinically relevant background for interrogating molecular pathways involved in tumor progression and metastasis.
CD300LD encodes an inhibitory leukocyte receptor containing immunoreceptor tyrosine-based inhibitory motifs (ITIMs) in its cytoplasmic tail. Upon ligand binding??potentially phosphatidylserine or pathogen-derived motifs??the ITIMs are phosphorylated and recruit the tyrosine phosphatases SHP-1 and SHP-2. These phosphatases dephosphorylate downstream targets including SYK, PI3K, and AKT, leading to suppression of the PI3K-AKT signaling axis and attenuated NF-??B activation. CD300LD also interacts with adaptor proteins GRB2 and FYN and the lipid phosphatase SHIP, thereby integrating multiple inhibitory signals. This cascade negatively regulates myeloid cell activation and may shape immune responses in the tumor microenvironment.
In the HGC-27 gastric cancer model, CD300LD disruption enables dissection of how inhibitory immunoreceptor signaling influences tumor cell-intrinsic behaviors such as proliferation, migration, and apoptosis. The polyclonal knockout population allows for assessment of responses to cytokines like IL-4 and TGF-??, which are implicated in immune regulation and tumor progression. Given the metastatic origin of HGC-27, this model is particularly valuable for studying the role of CD300LD in gastric adenocarcinoma dissemination and immune evasion mechanisms.
Researchers can employ these polyclonal knockout cells for diverse functional assays, including western blotting for CD300LD and SHP-1/SHP-2, RT-qPCR to confirm gene disruption, proliferation and migration analyses, apoptosis detection, and phospho-protein profiling of PI3K-AKT and NF-??B pathways. Co-immunoprecipitation can probe interactions with SHP-1, SHP-2, SHIP, GRB2, or FYN. These applications facilitate functional genomics of CD300LD in gastric cancer, tumor immunology studies, drug target validation, and immune checkpoint research. For further details, please contact Ascent Research.
