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Panoply™ Human DKK1 Knockdown Stable Cell Line

For research use only. Not intended for any clinical use.

Cat. No. :   CSC-DC004327

Host Cell :   HEK293 (Hela and other cell types are also available) Validation :   Real-Time RCR

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Cell Line Information

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Gene Information

Cat. No. CSC-DC004327
Description Creative Biogene's Knockdown Cell Lines are target specific shRNA lentivirus transduced cells. The percent knockdown levels range from 75-99% depending on the gene, as evaluated by Real-Time RCR. Cells are rigorously qualified and mycoplasma free.
Target Gene DKK1
Host Cell HEK293 (Hela and other cell types are also available)
Host Cell Species Homo sapiens (Human)
Applications

(1) Studying gene functions

(2) Studying gene interactions and signaling pathways

(3) Target validation and drug discovery

(4) Designing diseases models

Size >1 × 106 cells / vial
Stability Validated for at least 10 passages
Validation Real-Time RCR
Quality Control Negative for bacteria, yeast, fungi and mycoplasma.
Storage Liquid Nitrogen
Shipping Dry Ice
Mycoplasma Negative
Format One frozen vial containing millions of cells
Storage Liquid nitrogen
Safety Considerations The following safety precautions should be observed.
1. Use pipette aids to prevent ingestion and keep aerosols down to a minimum.
2. No eating, drinking or smoking while handling the stable line.
3. Wash hands after handling the stable line and before leaving the lab.
4. Decontaminate work surface with disinfectant or 70% ethanol before and after working with stable cells.
5. All waste should be considered hazardous.
6. Dispose of all liquid waste after each experiment and treat with bleach.
Ship Dry ice
Gene Name DKK1 dickkopf 1 homolog (Xenopus laevis) [ Homo sapiens ]
Gene Symbol DKK1
Synonyms SK; DKK-1
Gene Description dickkopf homolog 1 (Xenopus laevis)
GeneID 22943
Uni ProtID I1W660
mRNA Refseq NM_012242.2
Protein Refseq NP_036374.1
Chromosome Location 10q11.2
Function growth factor activity; low-density lipoprotein particle receptor binding; protein binding; receptor antagonist activity; signal transducer activity;
Pathway Direct p53 effectors, organism-specific biosystem; Presenilin action in Notch and Wnt signaling, organism-specific biosystem; Regulation of Wnt-mediated beta catenin signaling and target gene transcription, organism-specific biosystem; Validated targets of C-MYC transcriptional repression, organism-specific biosystem; Wnt Signaling Pathway NetPath, organism-specific biosystem; Wnt signaling network, organism-specific biosystem; Wnt signaling pathway, organism-specific biosystem;
MIM 605189
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Pancreatic ductal adenocarcinoma (PDAC) is a major histological subtype of pancreatic cancer. Despite advances in surgery and systemic therapy, its 5-year survival rate remains below 10%, making it one of the deadliest solid malignancies. Here, researchers screened and externally validated four reproducible tumor-associated genes-DKK1, COL10A1, SULF1, and SLC24A3. DKK1 is primarily expressed in tumor epithelial cells and its expression changes with malignant progression. Spatially, DKK1 localizes to predominantly epithelial regions, revealing significant intratumoral heterogeneity and highlighting epithelial-endothelial and endothelial-immune signaling pathways in high-scoring regions. Immunodevolution analysis showed that high DKK1 expression was associated with increased myeloid infiltration and decreased cytotoxic lymphocyte characteristics. Functionally, DKK1 knockdown impairs cell migration, proliferation, and colony formation, while increasing apoptosis. These results indicate that DKK1 is an epithelial-derived regulator associated with malignant progression and tumor-stromal-immune remodeling, supporting its potential as a biomarker and therapeutic target for pancreatic ductal adenocarcinoma (PDAC), including its rational combination with stromal modulation strategies and immunotherapy.

To validate the function of DKK1 in pancreatic cancer cells, researchers knocked down DKK1 in MIA PaCa-2 and PANC-1 cells and assessed key malignant phenotypes. Wound healing assays showed that, compared to the control group, DKK1 knockdown cells exhibited reduced migration ability, resulting in delayed scratch healing (Figure 1A, B). Transwell assays also consistently showed a reduced number of migrating cells in DKK1 knockdown cells (Figure 1A, B). In addition to migration ability, DKK1 knockdown also reduced colony formation ability in colony formation assays (Figure 1C) and inhibited cell proliferation for up to four days in CCK-8 assays (Figure 1D, E).

Figure 1. Functional effects of DKK1 knockdown in pancreatic cancer cell lines.Figure 1. Functional effects of DKK1 knockdown in pancreatic cancer cell lines. (Xu J, et al., 2026)

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