The CD44 Knockout CAL-27 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population in which the CD44 gene has been disrupted using CRISPR/Cas9-mediated genome editing. This product provides a heterogeneous pool of cells with loss-of-function alterations in CD44, delivering a physiologically relevant model for studying CD44-dependent processes in a human oral cancer background. The polyclonal format retains the genetic diversity inherent to the editing process, making it suitable for experiments that benefit from population-level effects rather than clonal homogeneity. The knockout model is derived from the well-characterized CAL-27 host cell line and is intended for use in advanced biomedical research investigating cell adhesion, migration, and oncogenic signaling.
The parental CAL-27 cell line is an epithelial cell line established from a human tongue squamous cell carcinoma, widely employed as a model for head and neck squamous cell carcinoma (HNSCC). CAL-27 cells exhibit typical features of aggressive carcinomas, including robust migratory and invasive capacities, making them a valuable platform for dissecting molecular mechanisms underlying oral cancer progression. The epithelial origin of this line is particularly relevant for studying cell adhesion receptor function, as these cells retain key cell-cell and cell-matrix interaction properties. By introducing a CD44 knockout into this genetically defined background, researchers gain a powerful tool to interrogate the specific contribution of CD44 to oncogenic phenotypes without altering the broader genetic context of HNSCC.
CD44 encodes a transmembrane glycoprotein that serves as the principal receptor for hyaluronic acid (hyaluronan) and also interacts with ligands such as osteopontin. Through its cytoplasmic tail, CD44 orchestrates intracellular signaling by coupling to the actin cytoskeleton via ERM proteins (ezrin, radixin, moesin) and recruiting Src family kinases. Canonical CD44-mediated signaling converges on the PI3K/Akt pathway, leading to activation of NF-??B, and on the Ras-MAPK cascade, resulting in ERK phosphorylation. This hub function enables CD44 to relay extracellular cues from hyaluronan, osteopontin, TGF-??, EGF, and estrogen to downstream effectors including Akt, ERK, RAC1, RHOA, MMP9, and ??-catenin. Consequently, CD44 regulates diverse cellular processes such as adhesion, migration, proliferation, and epithelial-mesenchymal transition by integrating signals from the tumor microenvironment.
In the CAL-27 oral squamous cell carcinoma context, CD44 expression is frequently associated with enhanced metastatic potential and therapy resistance. Knockout of CD44 in these cells is anticipated to impair hyaluronan-dependent adhesion, attenuate PI3K/Akt and ERK signaling, and reduce the activity of matrix metalloproteinases like MMP9, thereby diminishing invasive capacity. This model enables dissection of CD44??s role in oral cancer stem cell maintenance and in the epithelial-mesenchymal transition program that drives tumor dissemination. The polyclonal nature of the knockout population mimics the heterogeneous CD44 loss observed in tumor subclones, providing a more realistic system for evaluating targeted therapies that aim to interfere with CD44 function.
Typical research applications include cell adhesion and migration assays, such as hyaluronan-binding assays and wound healing or transwell migration studies, where CD44-dependent motility can be quantified. This model is also well-suited for western blot analysis of EMT markers, flow cytometric monitoring of CD44 surface expression loss, and functional evaluation of CD44-targeted agents. It supports mechanistic studies on drug resistance in HNSCC, as CD44 signaling contributes to chemoresistance via Akt and NF-??B activation. For specific inquiries about this product, please contact Ascent Research.
