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Cat. No. ARG40274

EBAG9 Knockout HGC-27 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Stomach

  • Disease:

    Carcinoma

CRISPR/Cas9-edited polyclonal knockout of EBAG9 in the HGC-27 gastric carcinoma cell line. EBAG9 (RCAS1) is an estrogen-responsive ligand that triggers lymphocyte apoptosis, mediating immune evasion. Its expression is upregulated by ER?? and estradiol, and it acts through caspase-3/-9 pathways. This model is ideal for studying tumor-immune interactions and estrogen signaling in gastric cancer. Applications include co-culture apoptosis assays, expression analysis, and immune cell viability studies. Disruption of EBAG9 enables investigation of immune checkpoint mechanisms and screening for anti-tumor immunity modulators.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    HGC-27

    Sex of Donor

    Unknown

    Age

    Unknown

    Derived From Site

    Metastatic; Lymph node

    Gene Name

    EBAG9

    Gene Identifier

    NCBI Gene ID 9166

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    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 EBAG9 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HGC-27 gastric carcinoma cell line. This product features targeted disruption of the EBAG9 (estrogen receptor-binding fragment-associated antigen 9) gene, providing a versatile model for loss-of-function studies. The polyclonal nature ensures a heterogeneous pool of knockout variants, reflecting population-level genetic diversity. Cells are delivered as a living polyclonal pool, optimized for immediate experimental use in cancer immunology and signaling research.

HGC-27 is a human gastric carcinoma epithelial cell line originally established from a lymph node metastasis of a gastric adenocarcinoma. As a metastatic derivative, HGC-27 retains key characteristics of advanced gastric cancer, including invasive properties and responsiveness to microenvironmental cues. This cell line serves as a robust in vitro platform for investigating molecular mechanisms underlying tumor progression and immune interactions within the gastric cancer milieu.

EBAG9 encodes an estrogen-responsive protein, also known as RCAS1, that functions as a ligand for an as-yet-unidentified lymphocyte receptor. Activation of this pathway induces caspase-3- and caspase-9-dependent apoptosis in tumor-infiltrating lymphocytes, thereby promoting immune evasion. EBAG9 expression is upregulated by estrogen receptor alpha (ER??) and estradiol, linking hormonal signaling to immune escape. Putative interactions with Bcl-2 family proteins suggest additional regulatory nodes within the extrinsic apoptotic cascade. Thus, EBAG9 operates at the intersection of endocrine signaling and immune checkpoint-like mechanisms.

In HGC-27 cells, EBAG9 overexpression mirrors clinical observations in gastric cancer, where it contributes to lymphocyte apoptosis and reduced anti-tumor immunity. Disruption of EBAG9 in this context enables researchers to dissect how estrogen-driven immune suppression facilitates tumor growth. The knockout model is particularly valuable for assessing changes in susceptibility to T-cell- or NK-cell-mediated killing, and for exploring the re-engagement of cytotoxic immune responses following loss of this immunomodulatory factor.

This polyclonal knockout population supports a wide range of experimental applications, including co-culture apoptosis assays with peripheral blood lymphocytes, RT-qPCR and western blotting for target engagement validation, flow cytometry-based immune cell viability assessments, and tumor xenograft studies to evaluate immune infiltration. It is an ideal tool for therapeutic target validation, screening of immune-modulating compounds, and mechanistic investigations into estrogen-driven immune evasion. For more information or custom requests, please contact Ascent Research.

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