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Cat. No. ARG40640

EFEMP1 Knockout huh-7 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Liver

  • Disease:

    Hepatocellular carcinoma

EFEMP1 Knockout Huh-7 Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout population in the Huh-7 hepatocellular carcinoma background for investigating loss-of-function of the ECM glycoprotein fibulin-3 (EFEMP1). Disruption of EFEMP1 alters ECM organization, integrin signaling, and potentiates TGF-?? pathway activity, impacting downstream effectors including Akt and ERK to modulate proliferation and migration. This model supports research on hepatocellular carcinoma progression, epithelial-mesenchymal transition, tumor microenvironment remodeling, and ECM biology. Compatible assays encompass western blotting, immunofluorescence, proliferation and migration analyses, ECM adhesion, xenograft models, and RNA-seq. For inquiries, contact Ascent 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

    EFEMP1

    Gene Identifier

    NCBI Gene ID 2202

    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 EFEMP1 Knockout Huh-7 Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population derived from Huh-7 hepatocellular carcinoma cells. This gene-disruption model enables functional investigation of EFEMP1 (fibulin-3) loss in a liver epithelial background. As a polyclonal pool, it captures a spectrum of editing events, avoiding clonal selection and providing a robust experimental system for population-level analyses.

The Huh-7 parental line, established from a 57-year-old Japanese male with hepatocellular carcinoma, is a widely used epithelial model in liver cancer research. These cells retain hallmark signaling pathways and ECM interaction profiles of hepatocyte-derived tumors, making them an appropriate host for studying ECM glycoprotein function.

EFEMP1 encodes fibulin-3, an ECM glycoprotein that contributes to basement membrane integrity and modulates adhesion, migration, and proliferation. It interacts with TIMP3, collagen IV, fibronectin, and laminin, while its expression is controlled by SP1, TGF-??, and miR-29. Downstream, EFEMP1 influences MMP activity, integrin signaling, and the activation of Akt and ERK, intersecting with PI3K-Akt, MAPK, and focal adhesion pathways. In this knockout model, disruption of EFEMP1 is expected to perturb ECM organization, enhance TGF-?? pathway output, and alter integrin-mediated downstream events.

In hepatocellular carcinoma, EFEMP1 often acts as a tumor suppressor, and its deletion may promote proliferation and migration through dysregulated ECM-receptor interactions. This polyclonal knockout population thus represents a valuable tool for dissecting the fibulin-3-dependent mechanisms that constrain liver tumor progression. It allows researchers to examine how loss of ECM integrity influences signaling networks and phenotypic outcomes in a heterogeneous cell population.

Typical research applications encompass hepatocellular carcinoma progression, epithelial-mesenchymal transition, ECM biology, and tumor microenvironment studies. The cells are compatible with western blotting, RT-qPCR, immunofluorescence, cell migration and proliferation assays, ECM adhesion assays, xenograft models, and RNA-seq. This product offers a defined genetic system for probing EFEMP1-associated regulatory networks in hepatic malignancy. For further information, contact Ascent Research.

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