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Cat. No. ARG36410

ADAMTS14 Knockout MCF7 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Breast

  • Disease:

    Invasive breast carcinoma of no special type

The ADAMTS14 Knockout MCF-7 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population in which ADAMTS14 gene disruption impairs the proteolytic maturation of procollagen I and III. Derived from the ER+/PR+/HER2? MCF-7 breast adenocarcinoma line, this model enables investigation of metalloproteinase-dependent extracellular matrix remodeling and collagen fibrillogenesis in cancer. ADAMTS14 functions downstream of TGFB1 and IL1B signals and interacts with procollagen I, procollagen III, and fibronectin to regulate collagen assembly. Loss of ADAMTS14 disrupts matrix integrity, affecting cell adhesion and migration. Suitable for breast cancer metastasis research, collagen processing assays, and matrix degradation studies, it supports Western blotting, invasion chambers, and immunofluorescence-based matrix analysis.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    MCF7

    Sex of Donor

    Female

    Age

    69 years

    Derived From Site

    Pleural effusion

    Gene Name

    ADAMTS14

    Gene Identifier

    NCBI Gene ID 140766

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    MEM (with NEAA)

    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 ADAMTS14 Knockout MCF-7 Polyclonal Cells comprise a population of MCF-7 cells engineered via CRISPR/Cas9-mediated gene disruption to eliminate functional ADAMTS14 expression. This polyclonal knockout product provides a loss-of-function model for investigating the role of the ADAMTS14 metalloproteinase in extracellular matrix remodeling and collagen homeostasis. The polyclonal format minimizes clonal biases and captures a diverse range of genetic alterations, enabling robust functional studies.

The parental MCF-7 cell line is an estrogen receptor-positive, progesterone receptor-positive, and HER2-negative human breast adenocarcinoma epithelial line isolated from a pleural effusion. It serves as a well-established model for luminal A breast cancer, retaining epithelial morphology and hormone responsiveness. MCF-7 cells are widely employed in cancer research to study cell adhesion, migration, and the molecular determinants of metastatic behavior, making them a suitable host for examining ADAMTS14-mediated matrix modulation.

ADAMTS14 is a secreted metalloproteinase that functions as a procollagen N-propeptidase, cleaving the N-propeptides of procollagen I and III to produce mature collagens required for fibril assembly. Its activity is regulated upstream by TGFB1 and IL1B, and its transcription is influenced by NFKB1 and SOX9. Within the extracellular matrix, ADAMTS14 interacts with procollagen substrates and fibronectin, and its proteolytic action governs the formation of collagen fibrils and overall matrix integrity. Consequently, ADAMTS14 knockout is predicted to disrupt collagen fibrillogenesis and downstream cell-matrix adhesion signaling.

In the MCF-7 breast cancer context, loss of ADAMTS14 impairs collagen maturation, leading to defective ECM organization that can alter cell adhesion, migration, and invasion??key processes in metastasis. This model enables dissection of how metalloproteinase-driven ECM remodeling influences the transition from an epithelial to a more motile phenotype. Furthermore, given ADAMTS14??s association with osteoarthritis and skeletal dysplasia, the knockout cells may also be relevant for studying matrix pathologies in joint and bone diseases.

Key applications include collagen processing studies, ECM dynamics in cancer, and breast cancer metastasis research. Representative assays such as Western blotting for ADAMTS14 and collagens, procollagen cleavage assays, cell invasion/migration Boyden chamber assays, and collagen fiber immunofluorescence allow direct evaluation of ADAMTS14 function. RT-qPCR for ECM genes and zymography for gelatinase activity further complement analysis of matrix remodeling. For technical inquiries and ordering, please contact Ascent Research.

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