The KRT20 Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human gastric adenocarcinoma cell line AGS, engineered for loss of keratin 20 expression. This heterogeneous knockout model disrupts KRT20 function without specification of the editing outcome, enabling robust analysis of intermediate filament biology and drug response in gastric cancer.
The AGS cell line, established from a patient-derived gastric adenocarcinoma, serves as a well-characterized model for studying gastric cancer proliferation, invasion, and therapeutic sensitivity. These adherent epithelial cells maintain key features of gastric carcinoma and support high-throughput screening and detailed molecular analyses, making them an ideal host for CRISPR/Cas9-mediated gene disruption in a disease-relevant context.
Keratin 20 (KRT20) is a type I intermediate filament protein predominantly expressed in differentiated gastrointestinal epithelia, where it forms heteropolymers with KRT8 to maintain cytoskeletal integrity. Its transcription is regulated by CDX2, GATA4, GATA6, and HNF4A, and is influenced by Wnt and Notch pathways. KRT20 interacts with plectin, desmoplakin, and epiplakin, linking filaments to desmosomes and hemidesmosomes. Disruption of KRT20 compromises intermediate filament organization, impairing cell adhesion, migration, and cytoskeletal dynamics, and potentially altering epithelial differentiation programs. These molecular changes can modulate downstream signaling cascades that integrate structural and transcriptional responses.
In AGS gastric cancer cells, KRT20 loss is expected to disrupt epithelial barrier function and shift the balance between proliferation and differentiation, promoting a more dedifferentiated or mesenchymal-like phenotype. This facilitates studies on epithelial-mesenchymal transition (EMT) and metastatic behavior. Moreover, cytoskeletal disruption can affect drug sensitivity and resistance by influencing apoptosis signaling and intracellular trafficking, offering a platform to examine how intermediate filament perturbations re-program therapeutic responses in gastric cancer.
This polyclonal knockout product is suited for diverse assays, including Western blot and RT-qPCR to confirm KRT20 ablation, immunofluorescence staining to visualize filament reorganization, scratch wound healing and Transwell migration assays to assess motility, and cell adhesion assays to measure attachment. Drug sensitivity profiling with MTT and apoptosis detection by Annexin V can reveal altered vulnerability, while RNA sequencing enables transcriptome-wide insight into KRT20-dependent networks. These applications support investigations into gastric cancer progression, biomarker validation, and therapeutic target identification. For further details, please contact Ascent Research.
