The DNAJC13 Knockout HGC-27 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population in which the DNAJC13 gene has been disrupted to generate a loss-of-function model. This product comprises a heterogeneous pool of HGC-27 cells carrying targeted gene disruptions introduced by CRISPR/Cas9, providing a powerful tool for investigating DNAJC13-dependent functions in a gastric cancer background. The polyclonal format allows immediate use in pooled functional assays without the need for clonal expansion, enabling robust and reproducible analysis of DNAJC13??s role in endosomal trafficking and disease-relevant pathways.
The HGC-27 host cell line is a poorly differentiated, epithelial cell line derived from a lymph node metastasis of a human gastric adenocarcinoma. This metastatic origin renders HGC-27 cells particularly valuable for studying the molecular mechanisms of gastric cancer invasion, migration, and metastatic spread. The cells retain many characteristics of advanced gastric cancer, including deregulated signaling networks, making them an appropriate model for evaluating the consequences of DNAJC13 loss on cancer cell behavior and for identifying potential therapeutic targets.
DNAJC13 encodes a co-chaperone that functions alongside Hsc70 (HSPA8) to regulate endosomal protein sorting via the retromer complex. It directly interacts with HSPA8, VPS35, SNX1, SNX2, and LRRK2, and sits at the interface of clathrin-mediated endocytosis and retromer-mediated retrograde transport. The protein??s activity is modulated by the Hsc70 ATPase cycle and endosomal phosphoinositides, and it governs critical downstream processes such as mannose 6-phosphate receptor trafficking, cathepsin D maturation, and lysosomal enzyme sorting. Through these interactions, DNAJC13 helps maintain the fidelity of the endosomal?Clysosomal system and influences pathways linked to neurodegeneration and cancer.
In the context of HGC-27 gastric cancer cells, disruption of DNAJC13 is expected to impair retromer-dependent receptor recycling and lysosomal degradation, leading to altered signaling that may affect proliferation, migration, and apoptosis. Given DNAJC13??s association with Parkinson??s disease, this knockout model also offers a platform for exploring the cross-talk between cancer and neurodegenerative disease mechanisms. The poorly differentiated and metastatic phenotype of HGC-27 cells further enhances the utility of this model for dissecting how endosomal dysfunction contributes to aggressive cancer traits and for testing interventions that target the retromer or lysosomal pathways.
This polyclonal knockout cell population is suited for a wide range of experimental applications, including detailed endosomal trafficking studies, migration and invasion assays, apoptosis profiling, and drug screening for lysosomal dysfunction. Researchers can employ complementary techniques such as western blotting to monitor retromer component levels, immunofluorescence to visualize endosomal marker redistribution, flow cytometry to assess transferrin internalization kinetics, and RNA-seq to capture global transcriptional changes. The model is particularly valuable for Parkinson??s disease research, gastric cancer metastasis investigation, and functional validation of hits from genetic screens. For further details or custom requests, please contact Ascent Research.
