The CD44 Knockout 143B Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population featuring disruption of the human CD44 gene within the 143B osteosarcoma cell background. This product provides a versatile loss-of-function model for investigating the multifaceted roles of CD44 in cellular adhesion, signaling, and metastatic behavior. The polyclonal format represents a pooled population of edited cells, offering a broad representation of gene disruption events without single-cell cloning, suitable for studies where heterogeneous knockout efficiencies mirror population-level biological variability.
Hosted in the 143B cell line??a human osteosarcoma model characterized by a mutant TP53 tumor suppressor and pronounced metastatic capacity??these cells recapitulate key aspects of bone tumorigenesis and distal spread. The 143B line is widely employed in xenograft models of metastasis due to its aggressive growth and tropism for lung and bone. The presence of endogenous wild-type TP53 mutations in this line provides a relevant genetic context for evaluating tumor progression mechanisms that co-occur with p53 dysfunction, making it a compelling system for dissecting CD44-dependent contributions to malignancy.
CD44 functions as a principal receptor for hyaluronic acid and osteopontin, activating PI3K/AKT/mTOR and Ras/Raf/MEK/ERK pathways to promote survival, proliferation, and migration. Ligand binding triggers ERK1/2 and Akt phosphorylation, while CD44 interacts with ezrin, merlin, and Src kinases to couple to Rho GTPases including RhoA and Rac1, regulating cytoskeletal dynamics and invasion. CD44 also influences NF-??B/IKK signaling, modulating MMP expression and facilitating EMT. Upstream regulators include TNF-??, IL-1??, TGF-??, EGF, and osteopontin, which enhance CD44 expression and downstream functions.
In the 143B osteosarcoma context, CD44 contributes to the aggressive metastatic phenotype, including adhesion, migration, and colonization. Disruption of CD44 in this polyclonal knockout population enables interrogation of hyaluronan metabolism and signaling networks driving EMT, drug resistance, and tumor-stroma interactions. This model is valuable for mapping dependency on CD44-mediated PI3K/Akt and MAPK/ERK activation, and assessing the impact on Rho GTPase-driven cytoskeletal reorganization and MMP secretion. The polyclonal nature allows study of functional heterogeneity within the knockout population.
The knockout model supports applications such as analyzing CD44-mediated metastasis signaling, validating therapeutic candidates, and probing drug resistance mechanisms. Compatible assays include western blotting for phospho-ERK1/2 and phospho-Akt, migration and invasion assays, adhesion assays, flow cytometry, immunofluorescence, qRT-PCR, phospho-signaling analysis, proliferation and apoptosis assays, and xenograft tumorigenesis. For further information, contact Ascent Research.
