The CD34 knockout 769-P polyclonal cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human renal clear cell adenocarcinoma cell line 769-P, with targeted disruption of the CD34 gene. This pooled knockout culture provides a heterogeneous loss-of-function model suitable for population-level studies of CD34-dependent processes without clonal selection artifacts. The polyclonal format captures genetic diversity inherent in CRISPR/Cas9-mediated gene disruption across a bulk population, enabling robust analysis of CD34 functional impact in a kidney carcinoma background.
The 769-P cell line was established from a primary human clear cell adenocarcinoma of the kidney, representing an epithelial model of renal cell carcinoma (RCC). These cells retain key characteristics of the parent tumor, including epithelial morphology, making them a widely used platform for investigating RCC biology, drug responses, and tumor-stroma interactions. The 769-P line thus offers a clinically relevant host for studying the roles of CD34 in kidney cancer.
CD34 encodes a heavily glycosylated type I transmembrane glycoprotein that functions in cell adhesion and serves as a hematopoietic stem/progenitor cell marker. It mediates cell-cell adhesion via binding to L-selectin and orchestrates intracellular signaling by recruiting adaptor proteins CRKL, SHC, and Grb2. This leads to activation of downstream cascades including MAPK/ERK and PI3K/AKT pathways, resulting in actin reorganization and enhanced migration. CD34 transcription is regulated by GATA2, RUNX1, and SCL/TAL1, and modulated by G-CSF and VEGF, integrating external cues with adhesive and migratory responses.
In 769-P renal carcinoma cells, CD34 disruption is expected to impair cell adhesion, reduce migratory capacity, and potentially attenuate stem-like properties. As CD34 has been linked to tumor-initiating cells in several carcinomas, this knockout model enables dissection of CD34 contributions to renal cell carcinoma progression, epithelial-to-mesenchymal transition, and tumor microenvironment interactions. The 769-P CD34 knockout cells thus facilitate mechanistic studies into how loss of CD34 remodels signaling networks and influences malignant phenotypes.
This product supports diverse advanced research applications such as cancer stem cell biology, cell adhesion and migration studies, kidney cancer modeling, and tumor microenvironment investigations. Functional assays including wound healing, Transwell migration, and colony formation can quantify phenotypic changes, while flow cytometry and Western blotting confirm CD34 ablation and downstream signaling alterations. Xenograft tumor growth assays further permit evaluation of CD34??s role in tumor initiation and progression. For additional details or product inquiries, please contact Ascent Research.
