The DTNBP1 Knockout HGC-27 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HGC-27 human gastric carcinoma epithelial cell line. This product provides a heterogeneous pool of cells carrying targeted disruption of the DTNBP1 gene, enabling loss-of-function studies in a gastric cancer context. The polyclonal format preserves natural genetic variability, mimicking heterogeneous tumor cell populations and facilitating robust investigation of gene function without clonal selection artifacts.
HGC-27 is an adherent epithelial cell line established from the metastatic lymph node of a patient with gastric adenocarcinoma. It serves as a well-characterized model for studying gastric cancer tumorigenesis, metastasis, and epithelial cell biology. HGC-27 cells exhibit key features of gastric carcinoma, including active PI3K/AKT signaling and invasive potential, making them suitable for evaluating the role of dysbindin in cancer progression.
DTNBP1 encodes dysbindin, a core subunit of the biogenesis of lysosome-related organelles complex 1 (BLOC-1), which also includes BLOC1S1?C6, snapin, and pallidin. Dysbindin orchestrates lysosome-related organelle biogenesis and synaptic vesicle trafficking by interacting with the AP-3 adaptor complex and regulating neurotransmitter release. In gastric cancer cells, dysbindin is implicated in PI3K/AKT signal transduction. Growth factor stimulation triggers PI3K/AKT pathway activation, promoting AKT-mediated phosphorylation of downstream effectors such as GSK3?? and mTOR. Dysbindin directly interacts with AKT1 and myospryn, integrating BLOC-1 function with AKT signaling cascades that govern cell survival, proliferation, and cytoskeletal dynamics. Disruption of DTNBP1 is therefore predicted to impair lysosomal trafficking and attenuate AKT signaling, potentially leading to reduced phosphorylation of mTOR and GSK3?? and altered dopamine D2 receptor trafficking.
In HGC-27 cells, DTNBP1 knockout disrupts the BLOC-1 complex, offering a unique platform to dissect the intersection of organelle biogenesis and oncogenic signaling in gastric adenocarcinoma. Given the role of AKT hyperactivation in gastric cancer, this model enables systematic examination of how dysbindin deficiency modulates PI3K/AKT-driven tumorigenic processes, including anchorage-independent growth, migration, and metastasis. Furthermore, it allows exploration of non-neuronal functions of dysbindin in epithelial contexts, bridging gaps between neurobiology and cancer research.
These polyclonal knockout cells are ideally suited for investigating dysbindin??s contribution to gastric cancer progression, performing comparative analyses of BLOC-1 complex integrity in epithelial cells, and modeling molecular phenotypes associated with Hermansky?CPudlak syndrome type 7 and schizophrenia in a cancer-relevant background. Researchers can employ western blotting to assess AKT phosphorylation status, RT-qPCR to quantify DTNBP1 and downstream target expression, immunofluorescence to visualize lysosomal marker distribution, flow cytometry to measure apoptosis, and migration/invasion assays to evaluate metastatic potential. Drug sensitivity profiling with PI3K/AKT inhibitors can elucidate dysbindin-dependent therapeutic vulnerabilities. For further details or custom requests, please contact Ascent Research.
