The CD34 Knockout 143B Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the CD34 gene has been disrupted. This heterogeneous pool of 143B osteosarcoma cells lacks functional CD34 protein, providing a versatile model for interrogating CD34-dependent functions without the bias introduced by clonal selection. The polyclonal format preserves diverse genetic backgrounds, enhancing the reproducibility and translational relevance of experimental readouts.
The 143B human osteosarcoma cell line originates from a bone tumor and is widely employed as a model system for studying osteosarcoma pathogenesis, metastatic dissemination, and therapeutic responses. 143B cells display an aggressive phenotype and are routinely used in xenograft assays to evaluate tumor progression and in vitro settings to dissect signaling networks relevant to bone cancer biology.
CD34 encodes a transmembrane sialomucin that acts as a scaffold for adhesion and signaling complexes. In hematopoietic contexts, CD34 mediates stem cell homing to bone marrow by binding L-selectin and recruiting CrkL, Src kinases, and the PI3K/AKT and ERK cascades. Its expression is regulated by hematopoietic cytokines such as G-CSF, GM-CSF, IL-3, and thrombopoietin, as well as transcription factors RUNX1, GATA2, SCL/TAL1, and Notch1 ligands. Downstream, CD34 engagement promotes CXCR4 expression, integrin activation, and survival signals through phosphorylation of AKT and ERK. Interacting partners include Podocalyxin, PSGL-1, and ICAM-1, which further link CD34 to cell adhesion and migration processes.
In the 143B osteosarcoma background, the functional role of CD34 is less characterized but may influence cell adhesion, motility, or interactions with the bone tumor microenvironment. Disruption of CD34 in these polyclonal knockout cells enables researchers to dissect whether CD34 contributes to osteosarcoma metastatic behavior, integrin-mediated adhesion, or cross-talk with Notch signaling. Because 143B cells retain mesenchymal features, this model also permits exploration of CD34 in oncogenic stemness programs or epithelial-mesenchymal transition-like processes, providing a platform to validate CD34 as a molecular target in sarcomas.
Routine applications encompass flow cytometry to confirm CD34 ablation, cell adhesion and transwell migration/invasion assays, Western blotting for phosphorylation states of AKT, ERK, and Src, and RT-qPCR profiling of downstream transcriptional changes. The knockout cells are compatible with in vivo metastasis models using 143B xenografts, facilitating studies on tumor dissemination and colonization. By employing a polyclonal knockout population, researchers can achieve statistically robust data that reflect the complexity of tumor cell heterogeneity. For further technical details or to discuss custom assay development, please contact Ascent Research.
