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Cat. No. ARG41081

EIF5A2 Knockout AGS Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Stomach

  • Disease:

    Adenocarcinoma

EIF5A2 Knockout AGS Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal loss-of-function model of the EIF5A2 gene in the AGS human gastric adenocarcinoma cell line. EIF5A2 is a hypusine-dependent translation elongation factor that drives expression of oncogenic proteins including Cyclin D1, Snail, and Bcl-2, promoting proliferation and epithelial-to-mesenchymal transition. Its activity is regulated by MYC and mTORC1 signaling. Disruption of EIF5A2 abolishes translation of these targets, impairing gastric cancer cell growth, migration, and metastasis. This knockout pool is ideal for investigating translational control mechanisms, gastric cancer progression, and oncogene dependence, and for drug target validation through assays such as western blotting, proliferation assays, and xenograft studies.

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Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    AGS

    Sex of Donor

    Female

    Age

    54 years

    Derived From Site

    In situ; Stomach

    Gene Name

    EIF5A2

    Gene Identifier

    NCBI Gene ID 56648

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    Ham's F-12

    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

EIF5A2 Knockout AGS Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout population of the AGS human gastric adenocarcinoma cell line, in which the EIF5A2 gene is disrupted to ablate protein expression. This heterogeneous loss-of-function model avoids clonal artifacts, providing a pooled knockout cell product for robust functional studies. The CRISPR/Cas9-mediated gene disruption eliminates EIF5A2, enabling investigation of its roles in gastric cancer biology without the need for single-cell clone characterization.

The AGS cell line originates from an epithelial tumor of a gastric adenocarcinoma patient and is a standard model for studying gastric carcinogenesis and metastasis. These cells display aggressive growth characteristics, responsiveness to growth factors, and invasive properties, making them suitable for dissecting molecular mechanisms underlying gastric cancer progression. The epithelial nature of AGS cells renders them particularly relevant for examining epithelial-to-mesenchymal transition and migration.

EIF5A2 functions as a translation elongation factor that facilitates synthesis of proteins containing polyproline stretches and other ribosome-pausing motifs. Its activity strictly requires hypusination, mediated by deoxyhypusine synthase (DHPS) and deoxyhypusine hydroxylase (DOHH). EIF5A2 is transcriptional target of MYC and operates downstream of mTORC1, linking growth signals to protein synthesis. It interacts with ribosomal proteins, RPS3A, and eEF2 to drive translation of oncogenic mRNAs such as Cyclin D1, Snail, Bcl-2, c-Myc, and MMP9. Thus, EIF5A2 promotes proliferation, EMT, apoptosis inhibition, and migration.

In AGS gastric cancer cells, EIF5A2 knockout abolishes hypusine-dependent translation elongation of MYC-driven oncogenic transcripts, thereby impairing cell growth and invasive capacity. This model enables dissection of the eIF5A hypusination pathway and its cross-talk with mTORC1 and MYC networks in gastric adenocarcinoma. The resulting attenuation of Snail and MMP9 expression reduces mesenchymal traits, highlighting EIF5A2??s role in metastasis. The polyclonal knockout is advantageous for drug screening and systems-level analyses targeting the translational machinery.

This knockout product supports a wide spectrum of experimental applications, including western blotting for EIF5A2 and downstream targets (MYC, Snail, Cyclin D1), RT-qPCR, proliferation assays (MTS, BrdU), transwell migration/invasion, colony formation, and xenograft tumor studies. Advanced approaches such as RNA-seq, polysome profiling, immunoprecipitation for interaction partners (DHPS, DOHH), and hypusine detection offer deeper mechanistic insight. Applications span gastric cancer biology, oncogene dependence studies, drug target validation, and translational control research. For further inquiries, please contact Ascent Research.

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