The DKK1 Knockout KYSE-150 Polyclonal Cells product constitutes a CRISPR/Cas9-edited polyclonal knockout cell population featuring targeted disruption of the DKK1 gene in the human KYSE-150 esophageal squamous cell carcinoma (ESCC) line. This loss-of-function model enables precise investigation of DKK1-dependent signaling in a genetically relevant epithelial cancer context, providing a versatile tool for functional genomics and pathway dissection.
The parental KYSE-150 cell line was established from a poorly differentiated esophageal squamous cell carcinoma derived from a male patient. This adherent epithelial line retains key molecular and phenotypic characteristics of ESCC, including dysregulated WNT/??-catenin signaling and TP53 pathway alterations, making it a well-defined in vitro system for studying esophageal tumor biology and therapeutic responses.
DKK1 is a secreted antagonist of the canonical WNT signaling pathway. It binds to LRP5/6 co-receptors and the transmembrane proteins KREMEN1 and KREMEN2, triggering internalization of the receptor complex and preventing WNT ligand?Cmediated activation. Consequently, DKK1 inhibits ??-catenin stabilization and transcriptional activation of TCF/LEF-regulated target genes such as MYC, CCND1, and AXIN2. DKK1 expression is positively regulated by TP53 and TGF-?? signaling, while it is frequently silenced in ESCC by promoter hypermethylation, contributing to aberrant WNT pathway activation.
In the KYSE-150 background, DKK1 knockout serves as a powerful model to dissect the tumor-suppressive role of DKK1 and the consequences of its loss on WNT/??-catenin pathway hyperactivity. This system allows researchers to delineate how DKK1 disruption influences downstream effectors, including ??-catenin, MYC, and CCND1, and to link molecular alterations to cellular phenotypes such as proliferation, migration, and resistance to apoptosis. The polyclonal nature of the edited population preserves biological heterogeneity while ensuring robust knockout effects.
Typical applications include quantitative analysis of WNT pathway components via western blotting and RT-qPCR, transcriptome-wide profiling by RNA-seq, and functional assays such as Transwell migration/invasion, MTT proliferation, and flow cytometry?Cbased apoptosis detection. The cells are also suited for TOP/FOP reporter assays to measure ??-catenin/TCF transcriptional activity, co-immunoprecipitation studies of LRP6 interactions, and drug sensitivity screening of WNT inhibitors. For detailed experimental protocols and technical support, please contact Ascent Research.
