The CD300LD Knockout KYSE-30 Polyclonal Cells comprise a CRISPR/Cas9-mediated gene-disrupted polyclonal population in which CD300LD has been targeted for loss-of-function analysis within the human esophageal squamous cell carcinoma line KYSE-30. This polyclonal knockout model provides a heterogeneous pool of edited cells, enabling robust population-level assessment of CD300LD??s role in cellular signaling and cancer phenotypes without clonal bias.
The host cell line KYSE-30 was derived from a well-differentiated squamous cell carcinoma of the middle esophagus from a 64-year-old male patient. It retains epithelial morphology and oncogenic signaling features characteristic of esophageal squamous cell carcinoma, making it a widely employed in vitro system for preclinical esophageal cancer research.
CD300LD encodes a type I transmembrane receptor containing an immunoreceptor tyrosine-based inhibitory motif (ITIM)-like sequence. Upon activation, CD300LD recruits SHP-1 and SHP-2 phosphatases, which dephosphorylate key intermediates of the PI3K/AKT and MAPK/ERK cascades. Transcriptionally regulated by IL-1?? and TNF-?? through NF-??B, CD300LD suppresses cell cycle progression via p21 and Cyclin D1 modulation, and promotes apoptosis through Bcl-2/Bax regulation. Thus, CD300LD functions as an inhibitory checkpoint that attenuates proliferative and survival signaling.
Knockout of CD300LD in KYSE-30 removes this negative regulatory constraint, potentially hyperactivating PI3K/AKT and MAPK pathways and altering cell proliferation, apoptosis, and migration. This model is therefore essential for dissecting CD300LD??s tumor-suppressive functions and its interplay with the esophageal cancer microenvironment.
This polyclonal knockout cell population is applied in functional characterization of CD300LD, elucidation of ITIM-dependent inhibitory signaling, and identification of therapeutic targets. Compatible assays include Western blot for CD300LD and phospho-AKT, RT-qPCR, Annexin V/PI apoptosis assays, CCK-8 proliferation studies, Transwell migration/invasion, co-immunoprecipitation with SHP-1/2, and xenograft tumor models. For further details and validation data, please contact Ascent Research.
