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Cat. No. ARG36809

IL27 Knockout T47D Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Breast (mammary gland)

  • Disease:

    Ductal carcinoma

The IL27 Knockout T-47D Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout population of the T-47D human breast cancer cell line, a model of ER-positive luminal A breast carcinoma. Disruption of IL27 eliminates a cytokine that signals through IL27RA and gp130 to activate JAK1/JAK2 and STAT1/STAT3, driving T-bet-mediated Th1 responses and IL-10 production. This polyclonal product enables investigation of IL27??s immunomodulatory functions in breast cancer biology, including tumor-immune interactions and JAK/STAT pathway regulation. Applications include western blotting, RT-qPCR, ELISA, and co-culture immune assays. For further details, contact Ascent Research.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    T-47D

    Sex of Donor

    Female

    Age

    54 years

    Derived From Site

    Metastatic; Pleural effusion

    Gene Name

    IL27

    Gene Identifier

    NCBI Gene ID 246778

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    RPMI 1640

    Supplement(s)

    10% Fetal Bovine Serum, 10μg/mL Insulin, 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 IL27 Knockout T-47D Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout population of the human breast ductal carcinoma cell line T-47D, with targeted disruption of the IL27 gene. This polyclonal format maintains a heterogeneous mixture of cells containing diverse gene edits, offering a biologically relevant loss-of-function model while avoiding clonal artifacts. The knockout pool enables robust studies of IL27 signaling without the need for single-cell isolation, providing a practical tool for high-throughput or co-culture assays where population-level effects are studied.

The T-47D host cell line was established from a pleural effusion of a 54-year-old female with infiltrating ductal carcinoma of the breast and is a classic model of luminal A breast cancer, characterized by estrogen receptor (ER) positivity and hormone-dependent growth. These epithelial cells retain key features of the luminal subtype, including expression of luminal cytokeratins and responsiveness to estrogen and progesterone, making them a gold standard for investigating endocrine-related breast cancer biology and the tumor microenvironment.

IL27 encodes the p28 subunit of the IL27 heterodimeric cytokine, which pairs with EBI3 to signal through IL27RA and gp130 (IL6ST). This triggers JAK1/JAK2 activation, STAT1/STAT3 phosphorylation, and induction of T-bet (TBX21) and IL10. Upstream, IL27 is induced by IFNG, TLR4 agonists, and CD40LG; downstream, it regulates TBX21, IL10, IFNG, and SOCS3. Thus, IL27 orchestrates Th1 differentiation and anti-inflammatory responses, crucial for antitumor immunity.

In the context of T-47D ER-positive breast cancer, IL27 knockout enables functional studies of the cytokine??s role in tumor cell signaling and immune modulation. This model helps clarify how loss of IL27 perturbs JAK/STAT transduction, alters expression of downstream regulators like SOCS3, and affects tumor cell proliferation and interactions with immune effectors, contributing to a better understanding of breast cancer immune evasion.

This polyclonal knockout pool is suitable for western blotting to confirm IL27 protein loss, RT-qPCR for transcriptional profiling, ELISA for secreted cytokine measurement, and STAT phosphorylation flow cytometry to assess signaling. Co-culture immune assays allow investigation of tumor-immune crosstalk, and proliferation assays reveal growth effects. These cells facilitate studies in breast cancer immunology, immune checkpoint regulation, cytokine therapy development, and autoimmune disease modeling. For further information, please contact Ascent Research.

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