The DTNB Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HGC-27 human gastric adenocarcinoma line, engineered for disruption of the DTNB gene (dystrobrevin beta). This polyclonal pool provides a heterogeneous loss-of-function model suitable for studying DTNB-dependent cell behavior and signaling without clonal artifacts. CRISPR/Cas9-mediated gene disruption enables robust investigation of dystrobrevin beta function in an epithelial cancer context for diverse biochemical and cell-based assays.
The parental HGC-27 line was established from a lymph node metastasis of a poorly differentiated gastric adenocarcinoma, representing a widely used model of metastatic gastric carcinoma with hallmark TP53 and KRAS mutations. These genetic lesions drive aggressive tumor phenotypes and dysregulated proliferation, rendering HGC-27 cells particularly relevant for probing invasion, migration, and cytoskeletal dynamics that underlie cancer dissemination. DTNB knockout within this background permits dissection of dystrobrevin beta??s contributions to these malignant processes.
DTNB encodes dystrobrevin beta, a scaffold protein integral to the dystrophin-associated glycoprotein complex (DGC) that links the actin cytoskeleton to the extracellular matrix. Dystrobrevin beta interacts directly with dystrophin, utrophin, and alpha1- and beta-syntrophins, anchoring signaling factors such as nNOS and the adaptor Grb2. These interactions facilitate downstream activation of the PI3K-Akt cascade, regulated by mechanical stretch and transcriptionally controlled by MEF2 family factors. Disruption of DTNB perturbs DGC assembly and associated signaling, impacting focal adhesion and cytoskeletal organization.
In the HGC-27 gastric adenocarcinoma context, DTNB ablation offers a unique system to explore non-canonical DGC functions in epithelial cancer, particularly effects on adhesion, migration, and PI3K-Akt signaling. The concurrent TP53/KRAS mutations may synergize with DTNB loss to amplify metastatic potential. This model bridges muscular dystrophy research with gastric cancer biology, enabling cross-disease insights into dystrobrevin-dependent mechanisms.
This polyclonal knockout pool is amenable to Western blotting and co-immunoprecipitation for DGC validation, adhesion and Boyden chamber migration/invasion assays, immunofluorescence for focal adhesions, and phospho-Akt analysis. Transcriptomic profiling via RNA-seq further elucidates DTNB-driven networks. Applications include mechanistic studies of gastric cancer metastasis, drug screening for dystrophinopathies, and evaluation of cytoskeletal signaling in tumors. For further technical details or custom inquiries, please contact Ascent Research.
