The CCDC22 Knockout HGC-27 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population engineered to disrupt the CCDC22 gene in the human gastric carcinoma cell line HGC-27. This product provides a mixed population of knockout cells derived from a bulk editing approach, enabling loss-of-function studies of CCDC22 within a heterogeneous cellular context. As a gene-edited polyclonal pool, it is ideally suited for experiments requiring a broad representation of knockout events, avoiding clonal artifacts while maintaining the native cellular diversity of the parental line.
HGC-27 is a well-characterized human gastric adenocarcinoma cell line originally isolated from a lymph node metastasis. These epithelial cancer cells exhibit features typical of advanced gastric carcinoma, including dysregulated growth factor signaling and metastatic potential. The cell line serves as a robust model for studying gastric cancer biology, endosomal trafficking, and receptor-mediated signal transduction. The integration of a CCDC22 knockout into this background allows researchers to dissect the gene’s function directly within a clinically relevant gastric cancer framework.
CCDC22 functions as an essential scaffolding subunit of the conserved COMMD/CCDC22/CCDC93 complex, which orchestrates endosomal sorting and lysosomal degradation of internalized cargoes, most notably the epidermal growth factor receptor (EGFR). Upon EGF stimulation, this complex interacts with COMMD1-10, CCDC93, Rab GTPases, and ESCRT components to facilitate receptor ubiquitination and subsequent lysosomal targeting. Gene disruption of CCDC22 inactivates this complex, leading to impaired EGFR downregulation, sustained activation of downstream MAPK and AKT pathways, and reduced NF-??B inhibition due to defective I??B?? ubiquitination. The knockout consequently perturbs both receptor trafficking and transcriptional responses, providing a powerful tool for mechanistic interrogation.
In gastric cancer, EGFR signaling and endosomal recycling are frequently aberrant, contributing to uncontrolled proliferation and survival. The CCDC22 knockout in HGC-27 cells models a specific defect in the endosomal sorting machinery, allowing investigation of how disrupted receptor trafficking influences oncogenic signaling networks. Moreover, since CCDC22 is associated with the COMMD complex and copper homeostasis, this model enables exploration of metal ion regulatory roles in cancer. It also holds relevance for Ritscher-Schinzel syndrome, a rare neurodevelopmental disorder linked to CCDC22 mutations, offering a platform for comparative pathobiology studies.
Researchers can employ this polyclonal knockout population in diverse functional assays. Western blotting of phosphorylated and total EGFR, coupled with degradation kinetics, quantifies receptor turnover. Immunofluorescence co-staining for endosomal markers (EEA1, Rab5) and COMMD components visualizes trafficking defects. Co-immunoprecipitation assesses COMMD/CCDC22/CCDC93 complex integrity, while NF-??B luciferase reporter assays and flow cytometry for surface EGFR provide complementary readouts. RT-qPCR of downstream targets further delineates signaling alterations. Applied in cancer biology, signal transduction, and drug discovery, these cells support target validation and mechanistic dissection of endosomal regulation. For additional information and custom inquiries, please contact Ascent Research.
