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Cat. No. ARG41122

ELANE Knockout CaSki Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Uterus (cervix)

  • Disease:

    Squamous cell carcinoma

The ELANE Knockout Ca Ski Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from HPV-16 positive cervical carcinoma Ca Ski cells. This model disrupts the ELANE gene, encoding neutrophil elastase, a serine protease that degrades extracellular matrix components and modulates inflammatory and NETosis pathways. The cells are suitable for studying tumor microenvironment interactions and immune modulation in cervical cancer. ELANE is regulated by transcription factors CEBPA and SPI1 and cytokines such as TNF-??, and it targets matrix proteins and inflammatory mediators. This polyclonal pool enables assays for invasion, cytokine analysis, and elastase inhibitor screening. Contact Ascent Research for further details.

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Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    CaSki

    Sex of Donor

    Female

    Age

    40 years

    Derived From Site

    Metastatic; Small intestine

    Gene Name

    ELANE

    Gene Identifier

    NCBI Gene ID 1991

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    RPMI 1640

    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 ELANE Knockout Ca Ski Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Ca Ski human cervical carcinoma cell line. This product consists of a heterogeneous pool of cells harboring targeted disruptions in the ELANE gene, resulting in loss of neutrophil elastase function. The polyclonal format circumvents clonal selection biases, thereby preserving population-level diversity and providing a robust loss-of-function model for investigating ELANE biology in epithelial cancer.

The parental Ca Ski cell line is an HPV-16 positive human cervical carcinoma model with an epithelial morphology. These cells express the viral oncoproteins E6 and E7, which inactivate p53 and Rb, respectively, and are widely used for studying cervical cancer mechanisms. Their adherent growth and well-characterized signaling networks make them suitable for reproducible functional assays, including invasion and cytokine profiling.

ELANE encodes neutrophil elastase, a chymotrypsin-like serine protease that degrades extracellular matrix components such as elastin, collagen, and fibronectin. Beyond matrix remodeling, ELANE processes inflammatory mediators and promotes neutrophil extracellular trap (NET) formation. The gene is transcriptionally activated by myeloid factors CEBPA, SPI1, and RUNX1, and its expression is induced by cytokines G-CSF, TNF-??, and IL-8. Downstream, ELANE modulates levels of IL-8 and CD14 and cleaves histones, while its activity is counteracted by the inhibitor SERPINA1 (??1-antitrypsin). ELANE functionally interacts with MPO and PADI4 during NETosis. In the tumor microenvironment, neutrophil-derived elastase can alter stromal architecture and immune cell recruitment.

In Ca Ski cervical carcinoma cells, ELANE knockout enables dissection of the protease??s specific contributions to tumor invasion and inflammatory signaling. By eliminating elastase activity, researchers can assess changes in extracellular matrix degradation, cytokine secretion, and responses to inflammatory stimuli. The polyclonal pool offers a practical advantage for bulk assays and helps mitigate the effects of clonal adaptation, making it suitable for initial functional screens and inhibitor testing.

This knockout model supports diverse research applications, including investigation of tumor-associated neutrophil elastase in cervical cancer progression, evaluation of extracellular matrix remodeling in tumor invasion, and drug screening for elastase inhibitors. It is also applicable for studying inflammatory signaling in HPV-positive carcinoma. Typical characterization and functional assays include Sanger sequencing, Western blotting for ELANE, neutrophil elastase activity assays, Matrigel invasion assays, gelatin zymography, cytokine arrays, and RNA-seq. For further technical information, please contact Ascent Research.

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