The DMTN Knockout HGC-27 Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human gastric carcinoma cell line HGC-27, engineered for disruption of the DMTN gene. This knockout model provides a powerful tool for dissecting DMTN functions in gastric cancer biology without the clonal selection biases associated with single-cell-derived lines, thereby capturing the heterogeneous genetic background typical of tumor cell populations. The polyclonal format enables robust loss-of-function studies in a physiologically relevant cancer cell context, facilitating investigations into cytoskeletal organization and tumor progression.
The HGC-27 cell line was originally established from a lymph node metastasis of a gastric carcinoma and is widely utilized as an adherent epithelial model in gastric cancer research. HGC-27 cells retain key characteristics of malignant gastric epithelium, including active integrin-mediated signaling and actin cytoskeleton remodeling, making them an ideal host for studying DMTN-driven processes in metastasis and invasion. Their well-documented growth properties and compatibility with standard cell-based assays support reproducible functional experiments.
DMTN (Dematin) is an actin-binding protein that plays a critical role in coupling the actin cytoskeleton to the plasma membrane, thereby regulating cell shape, membrane stability, and cytoskeletal architecture. Mechanistically, DMTN acts downstream of Rho GTPases such as RhoA and Rac1, and is regulated by integrin signaling and the erythroid transcription factor GATA1. It directly interacts with spectrin, adducin, actin, and band 4.1 to orchestrate the assembly of the spectrin?Cactin network. Representative pathway components include the WAVE complex and Arp2/3, which cooperate with DMTN in actin nucleation and branching. Knockout of DMTN disrupts these interactions, leading to aberrant actin dynamics and compromised adhesion molecule function.
In HGC-27 gastric carcinoma cells, DMTN knockout disrupts actin cytoskeleton organization, impairing cell adhesion and migration??key processes in tumor invasion and metastasis. The well-characterized role of Rho GTPase signaling in gastric cancer progression makes this model particularly valuable for examining DMTN-dependent cytoskeletal alterations. The polyclonal knockout format minimizes clonal artifacts, better reflecting the heterogeneity of gastric tumors and supporting studies of DMTN function within a mixed population context.
Researchers can employ this DMTN knockout model in a variety of assays to probe cytoskeletal dynamics, including immunofluorescence staining for F-actin organization, Western blotting for interacting partners such as spectrin and adducin, and quantitative cell adhesion and transwell migration/invasion assays. The model is particularly suited for functional studies of tumor metastasis, drug target validation, and signaling pathway analysis in gastric cancer. In vivo, the polyclonal knockout cells can be used in xenograft tumorigenicity studies to evaluate the impact of DMTN disruption on tumor growth and metastatic potential. For further details and custom inquiries, please contact Ascent Research.
