The CD34 Knockout AGS Polyclonal Cells product provides a heterogeneous population of CRISPR/Cas9-edited AGS cells with targeted disruption of the CD34 gene. This polyclonal knockout cell pool serves as a loss-of-function model for investigating CD34-dependent mechanisms in a gastric adenocarcinoma background, enabling functional studies without clonal selection artifacts.
The AGS cell line, established from a gastric adenocarcinoma patient, is a widely employed epithelial model for studying gastric cancer pathogenesis, tumor microenvironment interactions, and therapeutic responses. Its well-characterized signaling networks and adherent growth properties make it suitable for CRISPR/Cas9-mediated gene disruption and downstream functional assays, including drug sensitivity profiling and migration studies.
CD34 is a transmembrane sialomucin that functions as a key adhesion molecule and is conventionally recognized as a hematopoietic stem cell marker. In non-hematopoietic contexts, CD34 engages L-selectin and couples to adaptor proteins such as CRKL and Crk, stimulating downstream pathways including PI3K/AKT and FAK/paxillin signaling. Upstream, CD34 expression is regulated by transcription factors GATA2, RUNX1, and ETS family members, as well as by epigenetic modifiers. Upon interaction with L-selectin, CD34 triggers integrin activation and cytoskeletal reorganization, promoting cell migration and survival. These molecular interactions position CD34 at the interface of cell adhesion and pro-survival signal transduction.
In the context of gastric adenocarcinoma, aberrant CD34 expression has been associated with tumor progression and stem-like properties. The AGS cell line, which expresses CD34, provides a relevant platform to dissect its contributions to epithelial adhesion, migration, and pro-survival signaling cascades. Disruption of CD34 in this background enables assessment of its role in cancer cell biology, including potential involvement in integrin-mediated interactions and PI3K/AKT pathway activation.
Researchers can employ these CD34 knockout polyclonal AGS cells to investigate CD34-dependent adhesion and migration using transwell migration assays, adhesion to extracellular matrix substrates, and flow cytometry-based profiling of surface integrins. The polyclonal population is also suitable for bulk RNA-seq to explore transcriptomic consequences of CD34 loss and for evaluating drug sensitivity in the absence of CD34-mediated survival signals. Additionally, this model supports studies of cancer stem cell characteristics and the validation of CD34 as a therapeutic target in gastric cancer. For further details or custom configurations, please contact Ascent Research.
