The DTNA Knockout HGC-27 Polyclonal Cells product comprises a heterogeneous population of HGC-27 gastric carcinoma cells engineered via CRISPR/Cas9-mediated disruption of the DTNA gene, generating a loss-of-function model for ??-dystrobrevin. This polyclonal knockout format bypasses clonal selection, enabling functional studies in a background that retains natural genetic variability while abolishing DTNA protein expression. The use of polyclonal populations minimizes artifacts associated with single-cell clones and facilitates robust screening applications.
The HGC-27 cell line is a human poorly differentiated gastric adenocarcinoma cell line originally derived from a lymph node metastasis. It is extensively employed to model key aspects of gastric cancer biology, including invasion, metastasis, and the role of tumor suppressors. As an epithelial cell line, HGC-27 maintains characteristics relevant to cell?Cextracellular matrix interactions, integrin-mediated adhesion, and epithelial?Cmesenchymal transition, providing a physiologically pertinent context for studying dystrophin-associated complex function in cancer.
DTNA encodes ??-dystrobrevin, a core component of the dystrophin-glycoprotein complex (DGC) that mechanically couples the actin cytoskeleton to laminin in the extracellular matrix. It binds dystrophin, syntrophins (SNTA1, SNTB1/2), and the sarcoglycan complex while anchoring nNOS. Transcription is activated by MEF2C and suppressed by DNA methylation and miR-30, with mechanical stress also modulating expression. Downstream, DTNA loss disrupts DGC integrity, leading to mislocalization of nNOS, and aberrant activation of FAK, Src, RhoA, and PI3K/Akt signaling, which destabilizes focal adhesions and alters actin dynamics.
In the context of HGC-27 gastric cancer cells, DTNA knockout is predicted to significantly disturb DGC-mediated adhesion to laminin-rich matrices, thereby enhancing migratory and invasive behaviors through deregulated FAK/Src signaling. This model is particularly relevant for investigating the putative tumor-suppressive functions of dystrobrevin in gastric carcinogenesis, as disruption of the DGC has been implicated in the progression of certain epithelial cancers. Researchers can use this system to dissect how loss of DTNA impacts metastatic potential and to identify downstream effectors that mediate these phenotypes.
A broad range of experimental applications are supported by these polyclonal knockout cells. Researchers can validate DTNA deletion and probe signaling networks via Western blotting for ??-dystrobrevin, phospho-FAK, and phospho-Src. Functional assays include Transwell migration and invasion, wound healing, and cell adhesion on extracellular matrix substrates. Immunofluorescence microscopy enables visualization of DGC components such as dystrophin and ??-dystroglycan. Additional uses encompass RNA sequencing for global transcriptomic profiling, drug sensitivity screens, and phospho-signaling pathway analysis. For further information and technical support, please contact Ascent Research.
