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Cat. No. ARG40483

EDIL3 Knockout MES-OV Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Ovary

  • Disease:

    Ovarian serous cystadenocarcinoma

The EDIL3 Knockout MES-OV Polyclonal Cells are a CRISPR/Cas9-mediated polyclonal knockout of the EDIL3 gene in the MES-OV human ovarian cancer cell line, a mesenchymal model for metastasis and chemoresistance. EDIL3 encodes a secreted integrin ligand that binds ??v??3 and ??v??5 receptors, activating FAK, Src, PI3K/Akt, and ERK1/2 to promote adhesion, migration, and angiogenesis. This loss-of-function model enables dissection of EDIL3-mediated signaling in ovarian cancer. Applications include migration/invasion, adhesion, and angiogenesis assays, as well as phospho-protein analysis and xenograft tumor studies, making it a versatile tool for investigating integrin-driven tumor progression and for drug target validation in oncology research.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    MES-OV

    Sex of Donor

    Female

    Age

    53 years

    Derived From Site

    Ascites

    Gene Name

    EDIL3

    Gene Identifier

    NCBI Gene ID 10085

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    McCoy's 5A

    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 EDIL3 Knockout MES-OV Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the EDIL3 gene in the MES-OV human ovarian cancer cell line. This heterogeneous loss-of-function model provides a robust system for studying EDIL3-dependent processes without the need for single-cell cloning, making it suitable for scalable functional assays in a mesenchymal cancer background.

MES-OV cells were originally derived from ascitic fluid of a patient with ovarian cancer and exhibit a stable mesenchymal-like phenotype with features of epithelial-mesenchymal transition (EMT). They serve as a well-established model for ovarian cancer metastasis and chemoresistance, displaying high invasiveness and altered matrix interactions, which are clinically relevant for investigating the roles of secreted factors like EDIL3 in tumor progression.

EDIL3 is a secreted extracellular matrix protein that functions as a ligand for integrin receptors ??v??3 and ??v??5. Binding of EDIL3 to these integrins activates focal adhesion kinase (FAK), which subsequently stimulates Src, PI3K/Akt, and ERK1/2 signaling cascades. These pathways regulate cell adhesion, migration, and angiogenesis. EDIL3 expression is upregulated by HIF-1?? under hypoxic conditions and by TGF-?? during EMT, linking tumor microenvironmental cues to enhanced metastatic potential. Disruption of EDIL3 therefore abolishes key integrin-mediated signals.

In the MES-OV context, EDIL3 knockout directly interrogates the contribution of integrin ligand signaling to ovarian cancer aggressiveness. Loss of EDIL3 impairs ??v??3/??v??5-mediated FAK and Akt activation, leading to reduced cell migration and invasion. This model enables dissection of EDIL3-specific effects, exploration of compensatory mechanisms, and assessment of therapeutic vulnerabilities in FAK- and Src-dependent pathways.

This polyclonal knockout cell population supports a range of functional assays, including cell migration (Boyden chamber), adhesion, and angiogenic tube formation assays. It is compatible with Western blotting for phospho-FAK and phospho-Akt, immunofluorescence for integrin clustering, and RNA-seq transcriptional profiling. In vivo, these cells can be used in xenograft tumor models to evaluate metastatic growth. For further information, please contact Ascent Research.

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