The KRT7 Knockout 769-P Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population derived from the 769-P human renal epithelial carcinoma cell line, in which the KRT7 gene has been disrupted. This polyclonal format offers a heterogeneous pool of edited cells, enabling loss-of-function studies without clonal selection. CRISPR/Cas9-mediated gene disruption ablates KRT7 expression, allowing investigation of keratin 7 depletion in a cancer-relevant background.
The 769-P cell line originates from a human renal cell adenocarcinoma and is widely used as a kidney epithelial tumor model. These cells retain key features of renal epithelial carcinoma, including characteristic morphology and growth properties, making them suitable for mechanistic studies in renal cell carcinoma progression. The host background provides a disease-relevant context for examining KRT7 loss in kidney cancer.
KRT7 encodes keratin 7, a type II intermediate filament protein that forms heterodimers with type I keratins such as KRT18 and KRT19. These heterodimers assemble into filaments that interact with desmosomal components including desmoplakin, plakoglobin, and plakophilin, anchoring the cytoskeleton to cell junctions and maintaining epithelial integrity. Upstream, KRT7 expression is regulated by TP63 and AP-1 transcription factors, and modulated by EGF signaling and retinoic acid. Downstream, KRT7-containing filaments influence cytoskeletal organization, cell migration, and epithelial barrier function, while interacting with plectin to link to the actin cytoskeleton.
In renal epithelial carcinoma, KRT7 disruption may compromise structural support and alter mechanotransduction, potentially affecting tumor cell behavior. Since keratin 7 is expressed in certain renal cell carcinoma subtypes, its loss in 769-P cells provides a model to assess KRT7’s role in maintaining epithelial characteristics and to explore functional consequences during tumor progression. This knockout system helps dissect KRT7-dependent signaling networks and their impact on kidney cancer cell phenotypes.
This KRT7-knockout polyclonal cell population is suitable for epithelial-to-mesenchymal transition (EMT) studies, cancer cell migration and invasion assays using scratch wound healing or Transwell systems, and drug resistance mechanism research. It also supports diagnostic marker specificity validation and mechanotransduction experiments, with compatibility for western blotting, immunofluorescence, RT-qPCR, and cell stiffness measurements. For additional technical information, please contact Ascent Research.
