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Cat. No. ARG40487

EDIL3 Knockout huh-7 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Liver

  • Disease:

    Hepatocellular carcinoma

The EDIL3 Knockout Huh-7 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the Huh-7 hepatocellular carcinoma line. EDIL3 encodes DEL-1, a secreted glycoprotein that binds integrins ??v??3/??v??5, activating FAK/Akt/ERK pathways to promote adhesion and migration, and inhibits LFA-1-dependent leukocyte adhesion. This model enables functional studies of EDIL3 in liver cancer migration, invasion, and angiogenesis. Applications include Boyden chamber, Matrigel invasion, and tube formation assays, as well as Western blotting for phospho-FAK, Akt, and ERK, supporting drug target validation and tumor-immune interaction research.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    Huh-7

    Sex of Donor

    Male

    Age

    57 years

    Gene Name

    EDIL3

    Gene Identifier

    NCBI Gene ID 10085

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    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

The EDIL3 Knockout Huh-7 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the widely used Huh-7 human hepatocellular carcinoma cell line. This heterogeneous pool contains cells with targeted disruption of the EDIL3 gene, creating a robust loss-of-function model that avoids clonal selection biases. The product is supplied as live polyclonal knockout cells, ready for downstream applications.

The parental Huh-7 cell line originates from a well-differentiated liver tumor and is extensively employed in hepatocarcinogenesis research and hepatitis C virus replication studies. Huh-7 cells retain characteristics of malignant hepatocytes, including rapid proliferation, anchorage-independent growth, and tumorigenicity in vivo, thereby providing a clinically relevant context for exploring liver cancer biology.

EDIL3 encodes DEL-1, a secreted glycoprotein that binds integrins ??v??3 and ??v??5 and phosphatidylserine. This interaction triggers FAK/Src activation, leading to PI3K/Akt and ERK1/2 phosphorylation, which promotes cell adhesion, migration, and survival. DEL-1 also inhibits LFA-1-dependent leukocyte adhesion, providing anti-inflammatory effects. EDIL3 expression is induced by TGF-??, hypoxia (HIF1??), and NF-??B, while downstream it upregulates VEGF and MMP-2/9, key mediators of angiogenesis and invasion.

In hepatocellular carcinoma, EDIL3 overexpression correlates with aggressive tumor behavior and metastatic dissemination. The polyclonal EDIL3 knockout Huh-7 cells offer a powerful genetic model to examine the contributions of DEL-1 to liver cancer cell migration, invasion, and angiogenesis. Disruption of EDIL3 is expected to dampen integrin-mediated FAK/Akt/ERK signaling and reduce the secretion of pro-angiogenic factors such as VEGF, thereby providing a platform to investigate key molecular events in HCC progression.

Researchers can utilize this knockout pool in Boyden chamber and Matrigel invasion assays to quantitatively measure migratory and invasive potential, respectively. Western blot analysis of phosphorylated FAK (Tyr397), Akt (Ser473), and ERK1/2 (Thr202/Tyr204) allows direct assessment of signaling pathway activity. Tube formation assays evaluate angiogenic capabilities, while immunofluorescence and ELISA enable visualization and quantification of DEL-1 localization and secretion. For immune interaction studies, the LFA-1-dependent leukocyte adhesion assay can be employed. These cells are also suitable for drug target validation and high-throughput screening campaigns. Please contact Ascent Research for additional technical information.

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