The CD2AP Knockout HGC-27 Polyclonal Cells are a polyclonal population of HGC-27 gastric carcinoma cells harboring CRISPR/Cas9-mediated disruption of the CD2AP gene. This loss-of-function model eliminates CD2AP protein expression across a heterogeneous pool of edited cells, avoiding clonal artifacts and enabling robust functional studies. The polyclonal nature reflects the diverse editing outcomes typical of CRISPR pooled screening, preserving allelic diversity for comprehensive phenotypic analysis.
The HGC-27 cell line is an adherent epithelial cell line originally derived from a human gastric adenocarcinoma. It is extensively used in gastric cancer research to study tumor cell adhesion, migration, invasion, and chemotherapeutic responses. The HGC-27 background provides a clinically relevant platform for examining the contributions of specific genes, such as CD2AP, to gastric carcinoma progression and drug sensitivity.
CD2AP encodes a scaffold protein that bridges membrane receptors, including CD2, nephrin, and growth factor receptors, to the actin cytoskeleton and endocytic machinery. Its activation occurs downstream of T cell receptor engagement, nephrin clustering, TGF-?? receptor stimulation, and EGF receptor activation. CD2AP interacts directly with cortactin, CAPZ, and dynamin, and forms complexes with podocin and the PI3K p85 regulatory subunit. Through these associations, CD2AP orchestrates actin polymerization, receptor-mediated endocytosis, and signal transduction via the PI3K/Akt and TGF-??/Smad pathways. Consequently, CD2AP regulates cell adhesion, migration, and proliferation in multiple cell types, positioning it as a key integrator of extracellular cues.
Disruption of CD2AP in HGC-27 gastric carcinoma cells uncouples these scaffold functions, perturbing adhesion receptor trafficking, actin dynamics, and downstream signaling. Since CD2AP expression is frequently altered in gastric cancer, this polyclonal knockout model enables functional interrogation of its roles in tumor cell adhesion, migration, and invasion. The model allows direct assessment of TGF-?? and PI3K/Akt pathway dependencies, including potential effects on epithelial-mesenchymal transition and cell survival. The polyclonal format further permits investigation of pathway compensation and heterogeneity in cancer cell populations.
Researchers can apply a variety of assays to this product, such as western blotting and RT-qPCR for expression analysis, immunofluorescence to visualize cytoskeletal architecture, scratch wound and Transwell assays for migration and invasion, flow cytometry for apoptosis and phospho-Akt signaling, and co-immunoprecipitation to map protein complexes. Drug sensitivity screening (e.g., with cisplatin) can reveal CD2AP??s impact on chemoresistance. This model also supports comparative studies relevant to podocyte biology and Alzheimer??s disease pathology. Additionally, the polyclonal cells are well-suited for genetic screens and drug combination studies. For additional technical details, please contact Ascent Research.
