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Cat. No. ARG35778

IL27 Knockout A2780 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Ovary

  • Disease:

    Endometrioid carcinoma

The IL27 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the human epithelial ovarian cancer cell line A2780, disrupting the IL27 gene that encodes the interleukin-27 cytokine. This model enables loss-of-function studies of IL27-mediated JAK-STAT signaling, which is driven by the IL27RA/gp130 receptor complex and involves key signal transducers STAT1 and STAT3. Used to investigate tumor-immune interactions in ovarian carcinoma, these cells support assays such as phospho-STAT analysis, cytokine profiling, and co-culture experiments. Applications include dissecting Th1/Th17 regulation, IL10 induction, and the impact of tumor-derived IL27 on the ovarian tumor microenvironment.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    A2780

    Sex of Donor

    Female

    Age

    Unknown

    Derived From Site

    In situ; Ovary

    Gene Name

    IL27

    Gene Identifier

    NCBI Gene ID 246778

    Morphology

    Epithelial-like

    Growth Mode

    Adherent and suspension

    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 IL27 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the A2780 human epithelial ovarian cancer cell line, designed for loss-of-function studies of the IL27 gene. IL27 encodes interleukin-27, a cytokine that orchestrates immune regulation through a heterodimeric receptor composed of IL27RA and gp130 (IL6ST). Using CRISPR/Cas9-mediated gene disruption, these polyclonal cells provide a heterogeneous pool of edited cells, avoiding clonal selection artifacts while enabling robust interrogation of IL27-dependent signaling and tumor-immune crosstalk.

The parental A2780 cell line, originating from an untreated ovarian endometrioid adenocarcinoma, serves as an established model of ovarian carcinoma. These adherent epithelial cells retain key molecular features of ovarian cancer, including alterations in DNA repair and apoptotic pathways, and are widely employed to investigate tumor cell biology, drug responsiveness, and immune interactions within the ovarian tumor microenvironment.

IL27 functions by engaging its heterodimeric receptor to activate JAK-STAT signaling, predominantly through JAK1, JAK2, and TYK2 kinases that phosphorylate STAT1 and STAT3. Activated STAT1 and STAT3 transcriptionally regulate downstream targets including TBX21, IL10, SOCS1, and SOCS3. IL27 signaling is induced by upstream regulators such as LPS, IFN-??, CD40L, and transcription factors NF-??B, IRF1, and IRF8. It partners with EBI3 to form the functional cytokine, and its receptor complex shares the gp130 signal transducer with other IL-6 family cytokines. This pathway promotes Th1 differentiation and IFN-?? production while opposing Th17 responses and stimulating anti-inflammatory IL-10 secretion.

In the context of epithelial ovarian cancer, IL27 influences the immunological landscape by modulating the balance between pro-inflammatory and suppressive signals. A2780 cells express components of the IL27 signaling machinery, and knockout of IL27 in this line enables dissection of autocrine and paracrine cytokine effects on tumor cell behavior and immune cell recruitment. The model is particularly relevant for exploring how tumor-intrinsic cytokine production shapes the ovarian tumor microenvironment and for studying links to autoimmune conditions such as rheumatoid arthritis and inflammatory bowel disease, where IL27 plays regulatory roles.

This knockout product supports a broad range of experimental applications, including phospho-STAT1/STAT3 western blotting, RT-qPCR for TBX21 and IL10 transcript levels, flow cytometric analysis of surface receptors, and ELISA-based cytokine profiling. Co-culture systems with immune effectors can be designed to assess T-cell polarization and tumor cell killing, complemented by RNA-seq transcriptomic profiling to map global gene expression changes upon IL27 loss. These tools facilitate detailed investigation of JAK-STAT signaling dynamics, Th1/Th17 differentiation, and cytokine network interactions in ovarian cancer research. For additional product specifications and technical support, please contact Ascent Research.

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