The KRT7 Knockout DLD-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the KRT7 gene has been disrupted to eliminate keratin 7 expression. This product provides a heterogeneous pool of DLD-1 cells carrying diverse loss-of-function mutations in the KRT7 locus, generated without single-cell cloning, making it suitable for studying population-level effects of KRT7 ablation. The polyclonal format captures the variability inherent in CRISPR-mediated gene disruption while maintaining the overall loss of keratin 7 protein, offering a robust model for functional genomics and phenotypic screening.
The host cell line, DLD-1, is a well-characterized human colorectal adenocarcinoma epithelial cell line originally derived from a Dukes’ type C tumor. DLD-1 cells exhibit microsatellite stability (MSS) and harbor oncogenic mutations in APC and KRAS, reflecting key genetic drivers of colorectal cancer. These cells are widely employed as a colorectal cancer model to investigate tumor biology, intestinal epithelial barrier function, and metastatic progression.
KRT7 encodes keratin 7, a type II intermediate filament protein that contributes to the structural integrity of epithelial cells and is a well-established marker of glandular and transitional epithelia. Keratin 7 forms obligate heteropolymers with type I keratins, primarily KRT8 and KRT18, and anchors to desmosomes through interactions with desmoplakin and plakoglobin. The KRT7 network is regulated upstream by transcription factors such as TP63 and SOX9, as well as by TGFB1 and EGFR signaling pathways. Downstream, keratin filaments influence mechanotransduction by modulating focal adhesion kinase (FAK), SRC, and AKT activity, thereby linking cytoskeletal organization to cell migration and survival signals.
Disruption of KRT7 in DLD-1 colorectal cancer cells is expected to perturb the keratin intermediate filament network, potentially compromising epithelial structural resilience, cell-cell adhesion, and mechanosignaling. Given the role of keratin 7 in maintaining cytoskeletal architecture, its knockout may alter the migratory and invasive properties of these cells, providing a relevant model to study the contribution of intermediate filaments to colorectal cancer metastasis. The polyclonal knockout population enables investigation of how heterogeneous KRT7 loss influences epithelial-mesenchymal transition (EMT) dynamics and tumor cell plasticity in a genetically defined MSS background.
This KRT7 knockout model supports diverse research applications in cancer biology, including quantitative assessment of cell migration and invasion using wound healing and Transwell assays, analysis of EMT marker expression via RT-qPCR, and evaluation of phospho-signaling changes through Western blotting for FAK, SRC, and AKT. Researchers can further probe keratin network integrity by immunofluorescence, measure cell stiffness, and identify KRT7-dependent interacting complexes through co-immunoprecipitation with KRT8 and KRT18. Transcriptomic profiling by RNA-seq enables global gene expression comparisons in the absence of keratin 7, facilitating biomarker discovery and drug resistance studies. For further details and customized inquiries, please contact Ascent Research.
