The CD34 Knockout 786-O Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population with disruption of the CD34 gene in the 786-O human renal carcinoma line. This polyclonal pool consists of a heterogeneous mixture of CD34-deficient cells, providing a robust loss-of-function model that avoids clonal selection bias and supports functional studies in a genetically diverse background.
The 786-O cell line is derived from a primary clear cell renal cell carcinoma (ccRCC) and is a widely employed model for kidney cancer research. This adherent epithelial line harbors a truncating mutation in the von Hippel-Lindau (VHL) tumor suppressor gene, leading to constitutive stabilization of hypoxia-inducible factors (HIFs) and upregulation of downstream targets such as vascular endothelial growth factor (VEGF). 786-O cells are well characterized for studies of tumor angiogenesis, metabolic reprogramming, and signal transduction in the context of VHL-deficient ccRCC.
CD34 is a transmembrane glycoprotein originally identified as a hematopoietic stem cell marker, but it also functions as a cell adhesion molecule and is expressed on endothelial progenitors and certain tumor cells. CD34 facilitates cell-cell adhesion primarily through binding to L-selectin (SELL) and modulates cellular migration via CrkL-mediated actin cytoskeleton reorganization. The CD34 signaling axis involves upstream transcriptional regulators including GATA2, RUNX1, FLI1, and NOTCH, as well as hypoxia-driven VEGF. Upon engagement, CD34 interacts with the ezrin-radixin-moesin (ERM) proteins EZR and MSN, and recruits the adaptor protein CrkL (CRKL). CrkL then activates Rac1, leading to paxillin phosphorylation and dynamic actin remodeling, thereby promoting cell adhesion and migration.
In renal cell carcinoma, aberrant CD34 expression has been observed in subsets of tumors and is associated with tumor vasculature and potential cancer stem cell phenotypes. In the 786-O VHL-null background, CD34 expression may be influenced by the deregulated HIF/VEGF axis, making this knockout model particularly valuable for dissecting the contribution of CD34 to hypoxia-driven adhesion, migration, and tumor-endothelial interactions. By eliminating CD34 in this genetically defined ccRCC line, researchers can examine how loss of CD34 alters cell-matrix adhesion, integrin activation, and migratory capacity, and can probe the interplay between CD34 and the VEGF/NOTCH signaling network.
This CD34 polyclonal knockout cell product is suitable for a range of functional assays, including flow cytometry to confirm loss of surface CD34, western blotting, cell adhesion and transwell migration assays, colony formation assays, and transcriptomic analyses such as qRT-PCR and RNA-seq. Key applications include investigation of CD34-mediated adhesion and migration in renal carcinoma, evaluation of CD34 as a tumor endothelial marker, characterization of cancer stem cell properties, and drug sensitivity screening. The polyclonal nature of the knockout reduces clonal artifacts and allows assessment of population-level phenotypic effects. For additional technical details or ordering information, please contact Ascent Research.
