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Cat. No. ARG35880

IL3 Knockout CAL27 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Oral cavity (tongue)

  • Disease:

    Adenosquamous carcinoma

The IL3 Knockout CAL-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from the CAL-27 human tongue squamous cell carcinoma line, featuring disruption of the IL3 gene. IL-3 is a hematopoietic growth factor that binds IL-3R?? and CD131 to activate JAK2/STAT5 and PI3K/AKT pathways, regulating cell proliferation and survival. This model enables exploration of IL-3 autocrine/paracrine functions in head and neck cancer, immune cell crosstalk, and JAK/STAT-targeted therapies. Applications include phospho-STAT5 flow cytometry, proliferation/apoptosis assays, and cytokine profiling. Contact Ascent Research for details.

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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

    IL3

    Gene Identifier

    NCBI Gene ID 3562

    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 IL3 Knockout CAL-27 Polyclonal Cells are a polyclonal population of human CAL-27 tongue squamous cell carcinoma cells with CRISPR/Cas9-mediated disruption of the IL3 gene. This loss-of-function model retains polyclonal genetic heterogeneity, enabling unbiased assessment of IL-3-dependent phenotypes in cancer research.

The CAL-27 cell line, derived from a human tongue squamous cell carcinoma, is a widely used epithelial model for head and neck cancer biology. It recapitulates aggressive tumor features and serves as a platform for studying oncogenic signaling, tumor microenvironment interactions, and therapeutic interventions.

IL-3 is a hematopoietic growth factor that stimulates myeloid progenitor proliferation and differentiation. It binds the IL-3R?? (CD123)/CD131 heterodimer, activating JAK2 to phosphorylate STAT5 and STAT3, which promote expression of targets like Bcl-xL and Cyclin D1 for cell survival and cycle progression. IL-3 also triggers PI3K-AKT and RAS-MAPK/ERK pathways, enhancing growth and inhibiting apoptosis. In hematopoietic cells, IL-3 transcription is regulated by TCR activation, NFAT, and AP-1, mechanisms that may extend to epithelial tumor cells under certain conditions.

In head and neck cancer, IL-3 may participate in autocrine/paracrine loops influencing tumor proliferation and immune cell recruitment. Though primarily a hematopoietic factor, IL-3 and its receptor have been observed in solid tumors and stromal compartments. Disrupting IL3 in CAL-27 polyclonal cells enables dissection of endogenous IL-3 contributions to tumor cell survival, apoptosis resistance, and immune crosstalk, particularly via JAK2/STAT5 and PI3K/AKT signaling.

Representative assays for these polyclonal knockout cells include phospho-STAT5 flow cytometry, RT-qPCR for gene expression, proliferation and apoptosis assays, and cytokine array profiling. This model facilitates investigation of JAK/STAT pathway inhibitors and IL-3-driven paracrine effects in oral squamous cell carcinoma. For technical inquiries, contact Ascent Research.

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