The CCDC50 Knockout AGS Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal population derived from the AGS human gastric adenocarcinoma epithelial cell line, engineered for loss-of-function studies of the CCDC50 gene. This polyclonal knockout model provides a genetically heterogeneous pool of cells harboring targeted disruptions of CCDC50, enabling robust investigation of gene function without the clonal biases inherent in single-cell-derived lines. The product serves as a critical tool for dissecting CCDC50-mediated regulatory mechanisms in gastric epithelial biology and disease contexts.
The host AGS cell line is a widely used transformed gastric epithelial model isolated from a human gastric adenocarcinoma. These cells display characteristic proliferative and migratory properties reflective of malignant gastric epithelium and are extensively employed to study gastric cancer signaling networks, host?Cpathogen interactions during Helicobacter pylori infection, and pharmacological responses to therapeutic agents. The AGS background thus offers a pathophysiologically relevant system for examining the roles of tumor-associated genes in gastric carcinogenesis.
CCDC50 functions as a negative feedback regulator of NF-??B signaling through its interaction with NEMO (IKBKG) and the deubiquitinase A20 (TNFAIP3). By binding NEMO and facilitating A20-mediated removal of K63-linked polyubiquitin chains from IKK complex components, CCDC50 suppresses IKK activation and downstream NF-??B transcriptional responses. Upstream inflammatory stimuli such as TNF-?? and IL-1?? induce CCDC50 expression, thereby establishing a negative feedback loop that attenuates NF-??B activity. Additionally, CCDC50 modulates autophagy by associating with ubiquitinated cargo and autophagy receptors, including p62 and LC3, thereby influencing autophagic flux and cellular homeostasis. These dual functions position CCDC50 at the intersection of innate immune signaling and proteostatic quality control.
In the AGS gastric cancer context, disruption of CCDC50 is expected to alter NF-??B pathway dynamics and autophagy regulation, both of which are critically involved in tumor progression, chronic inflammation, and therapeutic resistance. Given the potential tumor-suppressive role of CCDC50, this knockout model allows researchers to explore how loss of CCDC50 may enhance proliferative signaling, migration, and survival in transformed gastric epithelial cells. The polyclonal nature of the knockout population further captures the heterogeneity of gene-editing outcomes, making it suitable for studying gene-dosage effects and population-level responses relevant to tumor evolution and drug sensitivity profiling.
This CCDC50 knockout model is ideally suited for a broad range of experimental applications, including NF-??B signaling pathway analysis via Western blotting of phosphorylated I??B?? and p65, luciferase reporter assays for NF-??B transcriptional activity, and immunofluorescence visualization of p65 nuclear translocation. Autophagy flux can be assessed through LC3 turnover assays, and protein interaction studies can be performed by co-immunoprecipitation of CCDC50 with NEMO or A20. Furthermore, the model supports functional assays such as migration/invasion, cell viability, and apoptosis analyses, as well as drug screening and H. pylori infection studies. For further details or inquiries, please contact Ascent Research.
