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Cat. No. ARG35342

ARG1 Knockout CAL27 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Oral cavity (tongue)

  • Disease:

    Adenosquamous carcinoma

The ARG1 Knockout CAL-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population from the CAL-27 tongue squamous cell carcinoma line, featuring disruption of the arginase-1 gene. ARG1 depletes arginine, impairing T-cell function via CD3?? downregulation and mTORC1 suppression, and is regulated by IL-4/STAT6, HIF-1??, and TGF-??. Disruption of ARG1 in this model enables study of arginine metabolism, immune evasion, and therapeutic targeting in head and neck cancer. Applications include arginase assays, T-cell proliferation studies, and metabolite profiling for drug discovery.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    CAL-27

    Sex of Donor

    Male

    Age

    56 years

    Derived From Site

    In situ; Tongue

    Gene Name

    ARG1

    Gene Identifier

    NCBI Gene ID 383

    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 ARG1 Knockout CAL-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population targeting the ARG1 locus in the CAL-27 human tongue squamous cell carcinoma line. This heterogeneous knockout pool allows loss-of-function studies of arginase-1 while avoiding clonal selection artifacts. The polyclonal nature ensures a diverse genetic background, enabling robust functional assays without the bias of single-cell-derived clones.

The parental CAL-27 line is an epithelial carcinoma derived from a male patient??s tongue squamous cell carcinoma, extensively used as a model for head and neck cancer. These cells maintain malignant traits such as sustained proliferation and invasiveness, and they recapitulate key metabolic and signaling features of oral cavity tumors. CAL-27 is thus an appropriate host for examining how arginine metabolism influences tumor progression and immune interactions in mucosal squamous cell carcinomas.

ARG1 encodes arginase-1, a hydrolase that converts L-arginine to L-ornithine and urea, reducing extracellular arginine and driving immune suppression. In the tumor microenvironment, arginine depletion downregulates CD3?? in T cells and inhibits mTORC1 signaling, impairing T-cell proliferation. ARG1 is induced by IL-4 and IL-13 through STAT6, and also regulated by C/EBP??, TGF-??, and HIF-1??. Ornithine downstream feeds polyamine synthesis, promoting tumor cell growth, while arginine competition with nitric oxide synthases modulates immune effector functions. Thus, ARG1 integrates immune evasion with metabolic reprogramming.

In CAL-27 oral cancer cells, ARG1-driven arginine catabolism is a key immunosuppressive mechanism. Disrupting ARG1 in this background allows dissection of how tumor-intrinsic arginine depletion shapes the microenvironment and whether restoration of arginine can reinvigorate T-cell responses. This polyclonal model is particularly suited for evaluating ARG1 as a therapeutic target in head and neck squamous cell carcinoma, where immune checkpoint blockade often meets resistance.

This product enables arginase activity assays, Western blot, RT-qPCR, and immunofluorescence for knockout validation. Co-culture with T cells can quantify proliferation and CD3?? expression, while metabolite profiling tracks arginine and ornithine levels. Migration and drug sensitivity assays support pharmacological studies of arginase inhibitors or immunotherapy combinations. For further information, please contact Ascent Research.

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