The CD24 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal HeLa cell population featuring targeted disruption of the CD24 gene. This knock-out model serves as a loss-of-function resource for interrogating the roles of CD24 in cancer biology, immunology, and signal transduction. The polyclonal format, generated by introducing Cas9 and guide RNA components into the host cells, yields a mixed population of edited alleles without single-cell cloning, enabling functional studies that reflect the heterogeneity of gene disruption events.
HeLa cells, the host line for this knockout, are an immortalized human cervical adenocarcinoma cell line harboring HPV18 integration and p53 inactivation. Widely utilized as a cancer cell model, HeLa cells provide a robust platform for investigating mechanisms of proliferation, metastasis, and drug response. Their well-characterized genetic background and ease of manipulation make them a standard choice for CRISPR-based gene editing and downstream phenotypic analyses.
CD24 encodes a glycosylphosphatidylinositol-anchored surface glycoprotein that functions as a co-receptor modulating cell adhesion, migration, and immune interactions. It binds ligands including P-selectin, Siglec-10, CD44, L1CAM, and VLA-4, and its transcription is regulated by SP1, E2F1, Notch, and Wnt, with further induction by IL-4 and TGF-??. Downstream, CD24 activates the Src/FAK and PI3K/AKT cascades, promoting integrin signaling, upregulation of cyclin D1, MMP2, MMP9, and anti-apoptotic Bcl-2 and Bcl-xL. CD24 signaling also intersects with MAPK/ERK, NF-??B, and Wnt/??-catenin pathways, collectively driving tumor cell proliferation, invasion, and immune evasion. Notably, the CD24?CSiglec-10 axis constitutes an immune checkpoint that transmits inhibitory signals to immune cells.
In HeLa cells, loss of CD24 is particularly significant for dissecting its contribution to malignant phenotypes. Derived from cervical adenocarcinoma and immortalized by HPV18, these cells provide a model for studying how CD24 modulates epithelial-mesenchymal transition, matrix degradation, and anoikis resistance. The knockout background is relevant for investigating CD24’s roles in multiple cancers??including breast, ovarian, pancreatic, and glioma??as well as in autoimmune conditions such as multiple sclerosis.
This CRISPR-edited polyclonal population supports a broad spectrum of experimental applications. Researchers can employ the knockout cells in assays such as Transwell migration and invasion, MTT or CCK-8 proliferation measurements, western blotting, flow cytometry for surface marker profiling, co-immunoprecipitation, immunohistochemistry, and transcriptomic analysis by RNA-seq. These approaches enable studies on tumor metastasis, drug resistance and sensitivity screening, immune checkpoint mechanisms, signal transduction analysis, and cancer stem cell characterization. For further technical information or to inquire about this product, please contact Ascent Research.
