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Cat. No. ARG36849

GPNMB Knockout TE1 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

GPNMB Knockout TE1 Polyclonal Cells are CRISPR/Cas9-edited polyclonal knockouts in human esophageal squamous cell carcinoma TE1 cells, disrupting the transmembrane glycoprotein GPNMB. This protein binds integrins ??v??3/??5??1 and syndecan-4, activating FAK/Src?CERK1/2 and AKT pathways to drive migration and invasion. The model enables mechanistic studies of GPNMB in esophageal cancer, including integrin signaling and stromal interactions. Applications include western blotting, Boyden chamber assays, phospho-protein analysis, and drug sensitivity testing. By comparing with parental cells, researchers can delineate GPNMB-dependent oncogenic programs and assess its therapeutic relevance.

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Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    TE1

    Gene Name

    GPNMB

    Gene Identifier

    NCBI Gene ID 10457

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    RPMI 1640

    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 GPNMB Knockout TE1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the human esophageal squamous cell carcinoma cell line TE1, designed to disrupt GPNMB expression. This loss-of-function model enables investigation of GPNMB-dependent processes in malignant esophageal epithelial cells. The polyclonal format preserves genetic diversity, allowing functional studies without clonal selection artifacts, and is suitable for assessing context-specific roles in adhesion, migration, invasion, and tumor-stroma interactions.

The TE1 cell line originates from a human esophageal squamous cell carcinoma and exhibits invasive characteristics typical of advanced disease. These cells serve as a canonical in vitro system for esophageal cancer research, faithfully recapitulating key features of tumor cell biology. The genetic background provides an ideal platform to evaluate the contribution of GPNMB to the malignant phenotype, including alterations in motility, proliferation, and therapeutic response.

GPNMB is a type I transmembrane glycoprotein that engages integrin receptors ??v??3 and ??5??1 and syndecan-4 to trigger intracellular signaling. Upon activation, it stimulates phosphorylation of FAK and Src, leading to downstream activation of ERK1/2 and AKT. These pathways drive expression of cyclin D1, c-Myc, and matrix metalloproteinases, thereby enhancing proliferation and invasion. GPNMB expression is regulated by MITF, TGF-??, and EGF, and it can intersect with TGF-??-Smad and PI3K-AKT-mTOR axes, positioning it as a central node in growth factor and adhesion signaling.

In esophageal squamous cell carcinoma, GPNMB overexpression correlates with aggressive behavior, making this knockout model valuable for mechanistic dissection. By comparing GPNMB-disrupted TE1 cells with parental controls, researchers can define its specific impact on ERK/MAPK and AKT/mTOR signaling, cytoskeletal reorganization, and cell-ECM adhesion. The model is well suited for probing GPNMB??s role in drug resistance and stromal communication, offering insights into its potential as a therapeutic target.

Applications include western blotting, RT-qPCR, RNA-seq, and functional assays such as Boyden chamber migration/invasion, proliferation, and phospho-protein analysis. Co-immunoprecipitation, immunofluorescence, and flow cytometry enable interaction and localization studies, while drug sensitivity tests assess therapeutic relevance. For technical inquiries, contact Ascent Research.

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