The CCDC50 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the CCDC50 gene in the HGC-27 human gastric cancer cell line. This product consists of a heterogeneous pool of cells with targeted gene disruptions, providing a robust loss-of-function model for functional genomics studies in gastric cancer. The polyclonal format mitigates clonal variation, ensuring more reliable representation of the knockout phenotype across experiments.
HGC-27 is a human gastric carcinoma cell line derived from a lymph node metastasis, serving as a widely used model for metastatic gastric cancer research. The cells maintain epithelial characteristics and express EGFR, rendering them responsive to EGF stimulation and suitable for studying EGFR-dependent signaling pathways. This clinically relevant background recapitulates features of invasive gastric cancer, enabling investigation of molecular mechanisms underlying metastasis and therapeutic resistance.
CCDC50 encodes a cytoplasmic adaptor orchestrating ESCRT-mediated endosomal sorting and lysosomal degradation of activated EGFR via interactions with TSG101 and VPS28, thereby attenuating MAPK1/3 (ERK) signaling. Additionally, CCDC50 modulates innate immune signaling by acting downstream of Toll-like receptor ligands (LPS, CpG DNA) and associating with TRAF6 to regulate NF-kappaB activation through the NFKB1/RelA complex, with NFKBIA (I??B??) providing negative feedback. The protein also engages ATG5 in autophagy and contributes to cytoskeletal dynamics, integrating upstream signals from EGF, TNF-alpha, and ubiquitination cascades.
In HGC-27 cells, knockout of CCDC50 enables interrogation of EGFR homeostasis and its role in gastric cancer progression. As this cell line originates from a metastasis, the model is apt for studying how defective EGFR downregulation contributes to invasive phenotypes and resistance to EGFR-targeted therapies. Moreover, disruption of CCDC50-mediated NF-kappaB regulation allows examination of tumor-intrinsic inflammatory signaling and its impact on metastatic behavior, offering a platform to explore therapeutic vulnerabilities in advanced gastric carcinoma.
Typical applications include western blotting for EGFR degradation and NF-kappaB activation, co-immunoprecipitation for CCDC50 interactions, immunofluorescence for EGFR trafficking, luciferase reporter assays for NF-kappaB activity, and RT-qPCR for downstream targets. Cell proliferation, migration, and flow cytometry-based apoptosis assays assess functional outcomes, while RNA-seq reveals transcriptomic consequences. These tools facilitate research on EGFR-targeted therapy resistance, gastric cancer metastasis, endosomal trafficking, autophagy, and inflammatory disorders. For technical inquiries, please contact Ascent Research.
