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Cat. No. ARG38828

DKK1 Knockout HAP1 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone Marrow

  • Disease:

    Chronic myeloid leukemia

The DKK1 Knockout CAL-27 Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout pool of CAL-27 human oral squamous cell carcinoma cells, disrupting Dickkopf-1 (DKK1), a secreted antagonist of Wnt/??-catenin signaling. DKK1 binds LRP5/6 and KREMEN co-receptors to promote ??-catenin degradation, reducing transcription of targets like c-Myc and Cyclin D1. This model enables Wnt pathway analysis, EMT and invasion assays, drug resistance profiling, and functional genomic studies in oral cancer. It is suitable for luciferase reporter assays, proliferation and apoptosis assays, and in vivo tumorigenicity experiments, serving as a critical tool for head and neck cancer research.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    HAP1

    Sex of Donor

    Male

    Age

    40 years

    Derived From Site

    Bone marrow

    Gene Name

    DKK1

    Gene Identifier

    NCBI Gene ID 22943

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    IMDM

    Supplement(s)

    10% Fetal Bovine Serum, 1% Penicillin-Streptomycin Solution

    Temperature

    37°C

    Atmosphere

    5% CO₂

  • Quality Control

    Sterility testing

    The bacterial, yeast, and fungi are not detected in these cells by daily monitor.

    Mycoplasma testing

    Negative for mycoplasma through PCR analysis

  • Disclaimer

    Intended Use

    This product is intended for laboratory in vitro use only. lt is not intended for diagnostic, therapeutic, or clinical applications.

    Disclaimer

    Ascent Research endeavors to provide accurate and up-to-date product information. However, no warranties or representations are made regarding its completeness or reliability. References to scientific literature and patents are for informational purposes only, and the customer assumes sole responsibility for verifying their accuracy.

    By accepting this product, the customer acknowledges and agrees to assume all risks associated with its receipt, handling, storage, disposal, and use, including compliance with all applicable safety and environmental regulations and precautions. Relevant laws, regulations, and ethical guidelines must be followed in conducting any research, modifications, or derivatives derived from this product.

    This product is provided "AS IS", and except as expressly stated herein, Ascent Research disclaims all other warranties, express or implied. Under no circumstances shall Ascent Research, its affiliates, or representatives be liable for indirect, incidental, consequential, or punitive damages arising from the use of this material. While Ascent Research employs rigorous quality control measures, we shall not be held responsible for damages resulting from misidentification or misinterpretation of the provided materials.

Description

The DKK1 Knockout CAL-27 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the CAL-27 human oral squamous cell carcinoma line, engineered for disruption of the Dickkopf-1 (DKK1) gene. This heterogeneous pool of edited cells offers a robust loss-of-function model without the need for clonal isolation, enabling comprehensive functional studies of DKK1 in a cancer-relevant epithelial background.

The parental CAL-27 cell line originates from a human tongue squamous cell carcinoma and serves as a widely characterized in vitro model for oral cancer research. CAL-27 cells retain key epithelial properties and exhibit invasive and metastatic behaviors, making them particularly valuable for investigating the molecular mechanisms underlying tumor progression, angiogenesis, and therapeutic resistance in head and neck cancers.

DKK1 is a secreted antagonist of Wnt/??-catenin signaling that binds LRP5/6 and KREMEN1/2 co-receptors to induce receptor internalization, preventing Wnt-Frizzled complex formation. This maintains ??-catenin destruction complex (AXIN, APC, GSK3??) activity, promoting ??-catenin degradation and suppressing TCF/LEF-driven transcription of targets such as c-Myc, Cyclin D1, and AXIN2. DKK1 expression is regulated by p53, ??-catenin/TCF, TGF-??, and glucocorticoids, integrating signals from PI3K/AKT, TGF-??, and NF-??B pathways.

In CAL-27 oral squamous cell carcinoma, DKK1 deletion disrupts Wnt signaling balance, which is often altered in head and neck cancers. This knockout model facilitates studies on how DKK1 affects tumor proliferation, epithelial-mesenchymal transition, and invasion via cross-talk with PI3K/AKT and TGF-??. Additionally, DKK1?CLRP5/6/KREMEN interactions are relevant to bone metastasis and tumor microenvironment modulation in tongue carcinomas.

Applications include Wnt luciferase reporter assays, Western blotting, RT-qPCR, and RNA-seq for pathway and gene expression analysis, as well as proliferation, wound-healing, Transwell invasion, and apoptosis assays to assess functional outcomes. The polyclonal pool is suitable for drug sensitivity screens, proteomic profiling, and in vivo xenograft tumorigenicity studies. For further information or technical support, please contact Ascent Research.

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