The CD300LD Knockout PaTu 8988t Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population of PaTu 8988t pancreatic cancer cells with targeted disruption of CD300LD. This loss-of-function model enables functional studies of CD300LD in tumor cell signaling and immune regulation. The polyclonal format preserves genetic diversity while eliminating CD300LD expression, avoiding clonal artifacts. CRISPR/Cas9-mediated gene disruption provides a robust system for interrogating CD300LD-dependent pathways.
The parental PaTu 8988t cell line is derived from a liver metastasis of pancreatic ductal adenocarcinoma and harbors an activating KRAS mutation. This genetic background reflects aggressive, metastatic disease with hyperactivated MAPK/ERK and PI3K/AKT signaling. PaTu 8988t cells are widely used to study pancreatic cancer biology, including drug resistance and immune evasion, making them a clinically relevant host for gene knockout studies.
CD300LD belongs to the CD300 family of immunoglobulin-like receptors with putative immune modulatory functions. It contains ITIM/ITAM-like motifs and interacts with DAP12 and Src family kinases. Ligand recognition, potentially of phosphatidylserine, triggers recruitment of SHP-1/SHP-2 phosphatases, modulating downstream PI3K, AKT, ERK1/2, and NF-??B pathways. Cytokine stimulation (e.g., IFN-??, TNF) regulates CD300LD expression, linking it to inflammatory tumor microenvironments. Thus, CD300LD integrates immune signals with tumor cell-intrinsic signaling networks that control proliferation, survival, and immune escape.
In PaTu 8988t cells, CD300LD knockout allows dissection of its role in KRAS-driven pancreatic cancer. Disruption of CD300LD permits analysis of its impact on phospho-AKT and phospho-ERK, proliferation, migration, and interactions with immune cells. This model is valuable for studying how CD300LD contributes to immune evasion and therapy resistance within the context of an oncogenic KRAS background, and for identifying pathway dependencies that may be therapeutically targeted.
Applications include immune checkpoint research, drug resistance mechanism studies, and tumor microenvironment investigations. Typical assays comprise Western blotting for CD300LD, phospho-AKT, and phospho-ERK; flow cytometry; proliferation and migration assays; immune cell co-culture; and RNA-seq transcriptomics. These approaches enable mapping of CD300LD signaling networks and testing of CD300LD-targeted interventions. For additional technical information, please contact Ascent Research.
