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Cat. No. ARG36411

AGGF1 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 AGGF1 Knockout MCF-7 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population in the MCF-7 breast epithelial line, offering a loss-of-function model for the secreted angiogenic factor AGGF1. AGGF1, activated by hypoxia via HIF1A, promotes AKT and ERK signaling and interacts with KRIT1, integrating PI3K-Akt and VEGF pathways. This product is suited for investigating AGGF1??s role in breast cancer angiogenesis, including paracrine signaling, target validation, and anti-angiogenic screening, using assays such as western blotting, phospho-protein analysis, and endothelial co-culture.

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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

    AGGF1

    Gene Identifier

    NCBI Gene ID 55109

    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 AGGF1 Knockout MCF-7 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the MCF-7 human breast epithelial cell line. This polyclonal pool comprises a heterogeneous mix of AGGF1-disrupted alleles, establishing a loss-of-function model suitable for investigating AGGF1-dependent processes without the artifacts of single-cell cloning. The polyclonal format provides a robust system for functional studies where population-level effects are desired.

The MCF-7 host line is an ER-positive, PR-positive, wild-type p53 human breast adenocarcinoma cell line originally derived from the pleural effusion of a patient with metastatic mammary carcinoma. It serves as a widely adopted model for hormone-responsive breast cancer research, offering well-defined signaling networks that facilitate the dissection of crosstalk between endocrine pathways and oncogenic mechanisms.

AGGF1 encodes a secreted angiogenic factor that is transcriptionally regulated by hypoxia through HIF1A. Following secretion, AGGF1 binds to endothelial cells and activates both the PI3K-Akt and MAPK/ERK signaling cascades, resulting in phosphorylation of AKT1 and ERK and consequent promotion of endothelial cell proliferation and migration. AGGF1 directly interacts with KRIT1, a protein critical for endothelial junction stability; disruption of this complex is linked to vascular malformations such as Klippel-Trenaunay syndrome. Thus, AGGF1 functions as a hypoxia-responsive mediator that couples HIF1A signaling to VEGF-dependent angiogenesis, with AKT1 and ERK serving as key downstream effectors.

In the context of MCF-7 breast cancer cells, knockout of AGGF1 enables precise interrogation of its role in paracrine angiogenic signaling. Researchers can determine whether ER-positive tumor cells require AGGF1 to stimulate endothelial cell responses and assess the dependency of AKT and ERK activation on AGGF1 in a hormone-sensitive background. This model also supports investigation of AGGF1-related vascular anomaly pathways and evaluation of anti-angiogenic therapeutic strategies.

Typical applications include western blotting and RT-qPCR for verifying AGGF1 ablation, phospho-specific analysis of AKT and ERK, co-culture endothelial tube formation assays, wound healing, Transwell invasion, and in vivo xenograft tumor studies. These polyclonal knockout cells therefore serve as a versatile tool for target validation, pathway dissection, and drug screening in breast cancer angiogenesis research. For further technical information or ordering, please contact Ascent Research.

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