The CAV1 Knockout 143B Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for loss-of-function studies of the CAV1 gene in a human osteosarcoma background. This product consists of a heterogeneous pool of 143B cells carrying targeted disruptions of the CAV1 locus introduced by CRISPR/Cas9, enabling investigation of caveolin-1-dependent signaling in a mesenchymal, metastatic tumor model.
The parental 143B cell line is a well-characterized human osteosarcoma model derived from the HOS line, known for its osteoblast-like, tumorigenic properties and thymidine kinase deficiency. These cells exhibit a mesenchymal phenotype and robust metastatic potential in vivo, making them an appropriate host for studying CAV1 functions in osteosarcoma progression, invasion, and metastasis.
Caveolin-1 (CAV1) is a major structural component of caveolae that acts as a scaffold protein, concentrating signaling molecules within plasma membrane invaginations. CAV1 directly interacts through its caveolin-scaffolding domain with Src family kinases, endothelial nitric oxide synthase (eNOS), epidermal growth factor receptor (EGFR), platelet-derived growth factor receptor (PDGFR), Ras GTPases, and integrin subunits, thereby regulating their activity. Upstream signals including TGF???, Src kinase, cholesterol, and mechanical stress modulate CAV1 expression and phosphorylation. Loss of CAV1 disrupts caveolar architecture and alters downstream pathways such as PI3K-Akt, Ras-ERK, focal adhesion dynamics, and eNOS activation, impacting integrin-mediated adhesion, growth factor signaling (e.g., EGFR, TGF???/SMAD), and mechanotransduction.
In the context of osteosarcoma, CAV1 exhibits context-dependent roles, functioning as either a tumor suppressor or a promoter of metastasis depending on cellular background and environmental cues. The CAV1 knockout 143B polyclonal cells, with their intrinsically high metastatic potential, offer a physiologically relevant platform to dissect these opposing functions. Eliminating CAV1 in this model system can help elucidate its contributions to focal adhesion turnover, ECM remodeling, and signaling crosstalk that drive osteosarcoma cell migration and invasion.
These polyclonal knockout cells are suited for diverse experimental applications, including phospho-signaling analyses (e.g., p-EGFR, p-Src, p-Akt), Transwell migration/invasion assays, adhesion assays, co-immunoprecipitation to probe scaffolding interactions, and transcriptomic profiling by RNA-seq. They can be employed to study CAV1-dependent drug resistance, mechanotransduction pathways, and tumor microenvironment interactions. For additional technical support or inquiries, contact Ascent Research.
