The CD300LD Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population carrying disruptive mutations in the CD300LD gene within the human A2780 ovarian carcinoma cell line. This heterogeneous knockout model enables loss-of-function analyses of the CD300LD inhibitory immunoreceptor while minimizing clonal bias. The polyclonal format provides a robust platform for dissecting CD300LD-dependent signaling in epithelial ovarian cancer.
The A2780 line originates from an untreated endometrioid adenocarcinoma patient and serves as a well-established model for high-grade serous ovarian carcinoma. Widely utilized for mechanistic studies of ovarian tumorigenesis and drug resistance, A2780 cells retain key oncogenic signaling features, including aberrant PI3K-AKT pathway activation. Their sensitivity to platinum-based agents, such as cisplatin, makes them particularly valuable for investigating molecular determinants of chemosensitivity and immune evasion.
CD300LD is a type I transmembrane protein with two ITIM motifs. Ligand engagement, possibly by phosphatidylserine, induces phosphorylation by Src kinases LYN and FYN. The phosphorylated ITIMs recruit SHP-1 (PTPN6) and SHP-2 (PTPN11) tyrosine phosphatases, which dephosphorylate the p85 subunit of PI3K, thereby suppressing AKT and mTOR activity. This inhibitory cascade also attenuates NF-??B signaling, positioning CD300LD as a negative regulator of growth factor and immunoreceptor-driven proliferation and survival.
In A2780 ovarian cancer cells, CD300LD likely tempers oncogenic signaling, and its ablation in this polyclonal knockout model is predicted to relieve ITIM-mediated suppression. Enhanced activation of the PI3K-AKT axis may promote cell proliferation, inhibit apoptosis, and alter migration capacity, offering a tractable system to study the role of inhibitory receptors in tumor aggressiveness. The model also permits exploration of how CD300LD influences cisplatin response, as AKT signaling modulates DNA damage repair and cell death decisions.
Researchers can confirm CD300LD knockout by Western blot or RT-qPCR and analyze pathway activation via phospho-AKT flow cytometry. Functional assays such as MTT, Annexin V, and Transwell migration/invasion allow phenotypic characterization. Cisplatin sensitivity testing further reveals the role of CD300LD in chemoresistance. This polyclonal knockout model is ideal for mechanistic studies of ITIM signaling, drug screening, and validation of CD300 family targets in ovarian cancer. Contact Ascent Research for more information.
