The KRT7 Knockout AGS Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population in which the KRT7 gene encoding keratin 7 has been disrupted via targeted CRISPR/Cas9-mediated gene disruption. This loss-of-function model is generated on the AGS human gastric adenocarcinoma cell line and delivered as a polyclonal pool, enabling robust and reproducible investigation of keratin 7 biology without clonal artifacts. The knockout population allows researchers to study the functional consequences of KRT7 depletion in an epithelial cancer context, facilitating dissection of keratin intermediate filament contributions to cellular architecture, adhesion, and signaling.
The AGS parental cell line was originally established from a gastric adenocarcinoma patient and displays adherent epithelial morphology, retaining features of gastric epithelial differentiation. As a widely employed model in gastrointestinal cancer research, AGS cells are valuable for examining oncogenic signaling, tumor microenvironment interactions, and drug response mechanisms. Their epithelial origin and tumorigenic properties make them particularly suitable for interrogating the role of intermediate filament proteins such as keratin 7 in maintaining epithelial homeostasis and in the progression of gastric malignancies.
Keratin 7 is a type II cytokeratin that forms obligate heteropolymers with keratin 8 (KRT8) to assemble intermediate filaments in simple epithelia. Its expression is regulated by retinoic acid receptors (RAR/RXR), GATA6, and SOX2, and influenced by TGF-??, EGFR, IL-1, and TNF-??. At the protein level, KRT7 binds desmoplakin, plakoglobin, plectin, and 14-3-3 proteins, anchoring filaments to desmosomes and hemidesmosomes and contributing to mechanical stability, cell shape, and migration. Cross-talk with integrin signaling through plectin and plakoglobin links the keratin network to adhesion and mechanotransduction. Disruption of KRT7 compromises this network, promoting epithelial-mesenchymal transition and invasive behavior.
In the AGS gastric adenocarcinoma model, loss of keratin 7 is predicted to impair intermediate filament integrity, diminishing mechanical resilience and altering cell?Ccell and cell?Cmatrix adhesion. This polyclonal knockout population provides a physiologically relevant platform to dissect how KRT7 deficiency influences gastric cancer hallmarks such as EMT-driven migration and invasion. It also enables exploration of signaling convergence from TGF-?? and EGFR onto the keratin cytoskeleton, and assessment of drug sensitivity changes linked to epithelial disruption.
This knockout tool is suitable for gastric cancer research, epithelial cell mechanics, and biomarker validation studies. Representative assays include western blotting for KRT7 and related keratins, immunofluorescence for filament architecture, wound-healing and transwell migration assays to quantify motility, Matrigel invasion for invasive potential, and omics approaches such as RNA-seq and phospho-proteomics to map signaling alterations. Cell viability, apoptosis, and adhesion assays further characterize functional outcomes. For additional technical details, please contact Ascent Research.
