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Cat. No. ARG40097

DVL2 Knockout A2780 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Ovary

  • Disease:

    Endometrioid carcinoma

DVL2 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population with disrupted DVL2, a key Wnt pathway scaffold. DVL2 transduces signals from Frizzled receptors, interacting with AXIN1 and GSK3?? to stabilize ??-catenin and drive TCF/LEF-mediated transcription of targets like MYC. This loss-of-function model enables dissection of Wnt-dependent processes in a human ovarian carcinoma background. The A2780 epithelial ovarian cancer line provides a cisplatin-sensitive platform for studying DVL2??s roles in proliferation, migration, and drug response. Applications include TOPFlash reporter assays, Western blotting, migration screens, and Wnt inhibitor testing for cancer research.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    A2780

    Sex of Donor

    Female

    Age

    Unknown

    Derived From Site

    In situ; Ovary

    Gene Name

    DVL2

    Gene Identifier

    NCBI Gene ID 1856

    Morphology

    Epithelial-like

    Growth Mode

    Adherent and suspension

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    DMEM

    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

DVL2 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the DVL2 gene has been disrupted, providing a loss-of-function model for investigating Wnt signaling. Derived from the A2780 human ovarian carcinoma line, this polyclonal population retains epithelial characteristics while lacking functional DVL2, enabling dissection of DVL2-dependent pathways. The polyclonal nature offers diverse editing events, suitable for population-based studies without single-cell cloning biases.

The A2780 cell line is a well-characterized human ovarian endometrioid adenocarcinoma model, established from an untreated patient with cisplatin-sensitive disease. As an epithelial ovarian cancer line, A2780 cells are employed in cancer biology, drug screening, and signal transduction research. Their intrinsic platinum sensitivity provides a context for evaluating how Wnt pathway perturbations influence chemotherapeutic responses in an oncogenic background.

DVL2 functions as a critical scaffold protein relaying signals from Frizzled receptors and LRP5/6 to multiple pathways. Upon Wnt ligand (e.g., Wnt3a, Wnt5a) binding, DVL2 is recruited to the membrane, polymerizes, and interacts with the ??-catenin destruction complex (AXIN1, APC, CK1, GSK3??) to disassemble it, stabilizing ??-catenin. Nuclear ??-catenin partners with TCF/LEF to activate targets like MYC and CCND1. DVL2 also signals to planar cell polarity via RhoA and Rac1, activates JNK and CaMKII/NFAT, and cross-talks with the Hippo pathway, demonstrating its regulatory breadth.

In A2780 ovarian cancer cells, DVL2 knockout uncouples Wnt-dependent proliferation, migration, and survival from the oncogenic network. This model is valuable for examining DVL2??s role in ovarian carcinoma progression and testing Wnt-targeted therapeutics. By eliminating endogenous DVL2, one can assess the impact on ??-catenin-responsive transcription, epithelial-mesenchymal transition, and cisplatin sensitivity, linking DVL2 function to clinically relevant phenotypes.

Applications include RT-qPCR of Wnt targets (MYC, CCND1), Western blotting for ??-catenin and DVL2, immunofluorescence for ??-catenin localization, and TOPFlash reporter assays. The polyclonal cells are suited for high-content Wnt modulator screening, proliferation (MTT) and migration assays, co-immunoprecipitation of DVL2 partners (AXIN1, GSK3??, ??-arrestin), and RNA-seq. These support mechanistic studies and drug discovery against Wnt-driven cancers. For further information, contact Ascent Research.

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