The KRT20 Knockout 769-P Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout population from the 769-P renal cell carcinoma line, designed for functional studies of keratin 20 (KRT20) in kidney cancer. This heterogeneous pool carries diverse KRT20 disruptions, enabling investigation of gene loss without clonal bias. The product provides a tractable model to dissect KRT20??s roles in epithelial biology and tumor progression within a clear cell renal carcinoma background.
769-P is a human renal cell carcinoma cell line derived from a primary clear cell adenocarcinoma, widely utilized as a model for clear cell renal cell carcinoma (ccRCC). Its kidney epithelial origin and characterized growth properties make it suitable for genetic manipulation and cancer phenotype assessment. The 769-P line offers a clinically relevant environment to examine how KRT20-dependent cytoskeletal changes influence oncogenic signaling, adhesion, and metastasis in renal malignancies.
Keratin 20, a type I intermediate filament protein, pairs with KRT8 to form cytoskeletal networks critical for epithelial integrity. KRT20 is transcriptionally activated by CDX2, GATA6, and Wnt/??-catenin, and its filaments interact with KRT18 and desmoplakin at desmosomes, linking to E-cadherin?C??-catenin adhesion complexes. Upstream regulators include retinoic acid and IL-6. Knockout of KRT20 disrupts these connections, potentially impairing cell?Ccell junctions and releasing ??-catenin for signaling, thereby modulating migration and invasion mediators.
In the 769-P renal carcinoma context, KRT20 expression??though atypical for adult kidney??can occur in aggressive tumor subsets. Its knockout enables exploration of how aberrant keratin filaments contribute to renal cancer cell plasticity. Disruption of the KRT20?CKRT8 network may weaken desmosomal adhesion and promote an EMT-like phenotype, facilitating studies on cytoskeletal reorganization, Wnt pathway crosstalk, and metastatic behavior. This model is valuable for interrogating KRT20??s role in renal tumor progression.
This polyclonal knockout cell population supports diverse assays, including immunofluorescence and western blotting for EMT markers (E-cadherin, vimentin), migration/invasion assays (Boyden chamber, wound healing), and cell adhesion analyses. Transcriptomic profiling via RNA-seq or RT-qPCR can delineate KRT20-dependent gene networks. The model aids in validating KRT20 as a biomarker or therapeutic target in renal and related cancers. For further details or technical support, please contact Ascent Research.
