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Cat. No. ARG35834

ADAMTS14 Knockout CAL27 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Oral cavity (tongue)

  • Disease:

    Adenosquamous carcinoma

The ADAMTS14 Knockout CAL-27 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout population derived from the CAL-27 human tongue squamous cell carcinoma line. This model targets ADAMTS14, a zinc metalloprotease that cleaves the N-propeptides of procollagens I, II, and III, a critical step in collagen fibrillogenesis and ECM organization. ADAMTS14 is activated by TGF??1 through the SMAD2/3 pathway and interacts with fibronectin and decorin. Its knockout in CAL-27 cells provides a tool for investigating collagen processing, ECM remodeling, and cancer cell invasion mechanisms. Suitable applications include migration assays, immunofluorescence, and ECM degradation studies. Contact Ascent Research for ordering.

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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

    ADAMTS14

    Gene Identifier

    NCBI Gene ID 140766

    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

ADAMTS14 Knockout CAL-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the CAL-27 human tongue squamous cell carcinoma line. This product provides a loss-of-function model for studying ADAMTS14, a zinc metalloprotease that functions as an aminoprocollagen peptidase, crucial for collagen maturation and extracellular matrix (ECM) organization. The CRISPR/Cas9-mediated disruption of the ADAMTS14 gene enables detailed investigation of its roles in collagen fibrillogenesis, ECM remodeling, and tumor microenvironment dynamics.

CAL-27 is an epithelial cell line established from a human tongue squamous cell carcinoma, serving as a robust model for head and neck cancer research. These cells exhibit characteristic features of invasive carcinoma, including altered cell adhesion and enhanced motility, making them particularly suitable for examining factors that regulate cancer cell behavior within the ECM-rich tumor microenvironment.

Mechanistically, ADAMTS14 specifically removes the N-terminal propeptides from fibrillar procollagens I, II, and III, encoded by COL1A1, COL1A2, and COL3A1. This cleavage is essential for collagen fibril assembly and subsequent crosslinking by lysyl oxidase (LOX), which determines tissue tensile strength. ADAMTS14 is transcriptionally regulated by TGF??1 through the SMAD2/3 signaling cascade, and it physically interacts with procollagens, fibronectin, and decorin in the ECM. Its activity thus directly promotes collagen processing and ECM structural integrity.

In the CAL-27 context, ADAMTS14 knockout likely impairs collagen maturation, leading to disrupted matrix architecture and altered cell?Cmatrix interactions. This may influence tumor cell invasion, migration, and metastatic potential, as ADAMTS14 has been implicated in osteoarthritis and musculoskeletal disorders, with emerging evidence suggesting a role in cancer progression. The model therefore offers a pathophysiologically relevant system to dissect how ECM remodeling affects squamous cell carcinoma aggressiveness.

This polyclonal knockout population is well-suited for a variety of research applications, including studies on collagen processing, ECM assembly, and tumor microenvironment remodeling. Representative assays compatible with this model include western blotting for N-propeptide cleavage, immunofluorescence staining of collagen I/III and fibronectin, Boyden chamber migration and invasion assays, and mass spectrometry-based collagen cross-linking analysis. Furthermore, it enables functional genomics screens and drug testing targeting ECM-related pathways. Researchers are encouraged to contact Ascent Research for further technical details and ordering information.

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