The CD300LD Knockout MCF-7 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population, generated by targeted disruption of the CD300LD gene in MCF-7 cells. This heterogeneous pool provides a loss-of-function model without single-cell cloning, maintaining genetic diversity and reducing clonal artifacts.
MCF-7 is a human breast epithelial adenocarcinoma cell line isolated from the pleural effusion of a metastatic breast cancer patient. It retains estrogen receptor (ER) expression and hormone responsiveness, serving as a well-characterized model for ER-positive breast cancer research, including hormone-driven proliferation and drug response studies.
CD300LD is a member of the CD300 immune receptor family, which includes receptors that signal via immunoreceptor tyrosine-based motifs and recruit phosphatases such as SHP-1 and SHIP-1, as well as Src family kinases. Although its exact function is uncharacterized, CD300LD may interact with lipids or other receptors, potentially modulating immune response genes. Knockout in MCF-7 disrupts these signaling interactions, enabling investigation of its role in cancer cell behavior.
This model is especially relevant for studying tumor-immune interactions, as the CD300 family is implicated in immune cell regulation. CD300LD knockout in an ER-positive breast cancer cell line allows researchers to explore how loss of an orphan immune receptor affects tumor cell proliferation, migration, and response to the microenvironment. This may reveal new insights into mechanisms of immune evasion in breast cancer.
Applications include validation by western blot or RT-qPCR, flow cytometric analysis of surface markers, and functional assays such as proliferation, migration/invasion, and drug sensitivity tests. Co-culture experiments with immune cells can assess cytokine secretion changes, directly testing the role of CD300LD in immune modulation. For more information, contact Ascent Research.