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Cat. No. ARG36440

HDAC8 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 HDAC8 Knockout MCF-7 Polyclonal Cells are a polyclonal CRISPR/Cas9-edited population disrupting HDAC8 in the estrogen receptor-positive MCF-7 breast cancer line. HDAC8 is a histone deacetylase that regulates chromatin and gene expression through deacetylation of histones H3/H4 and non-histone targets including SMC3 and p53, impacting cell cycle, DNA repair, and estrogen signaling. This knockout model is ideal for investigating HDAC8 in breast cancer biology, validating epigenetic drug targets, and studying cohesin acetylation. Applications include western blotting, RT-qPCR, ChIP-qPCR, and functional assays for proliferation, apoptosis, and drug sensitivity.

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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

    HDAC8

    Gene Identifier

    NCBI Gene ID 55869

    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 HDAC8 Knockout MCF-7 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the MCF-7 human breast adenocarcinoma line. This heterogeneous pool carries diverse loss-of-function mutations in HDAC8, providing a robust model for studying gene function without clonal bias. The polyclonal format ensures target-gene disruption across the population, making it suitable for investigating HDAC8 in a breast cancer context. These cells are ready for immediate use in epigenetic and drug discovery research.

MCF-7 is an epithelial cell line isolated from the pleural effusion of a metastatic breast adenocarcinoma patient. It expresses estrogen receptor alpha, serving as a key model for estrogen receptor-positive breast cancer. The cells retain hormone responsiveness and relevant signaling pathways, enabling studies of estrogen-driven proliferation, apoptosis, and epigenetic regulation. This background offers a physiologically relevant platform to examine the intersection of histone deacetylation and estrogen receptor biology.

HDAC8 is a class I histone deacetylase that deacetylates histones H3 and H4 and non-histone substrates SMC3, p53, and HSP90, promoting chromatin condensation and transcriptional repression. It regulates cell cycle progression, DNA repair, and apoptosis, and is controlled by the transcription factor MYC and inhibited by vorinostat and trichostatin A. Through interactions with SMC3, p53, and HSP90, HDAC8 links epigenetic modifications to cohesin dynamics, tumor suppressor stability, and protein homeostasis.

In MCF-7 cells, HDAC8 knockout disrupts histone acetylation homeostasis, impairing estrogen receptor signaling, cell cycle progression, and DNA repair. This model is valuable for dissecting HDAC8??s role in breast cancer pathogenesis and for exploring cohesin acetylation defects relevant to Cornelia de Lange syndrome. The polyclonal nature allows assessment of heterogeneous mutation outcomes, providing insight into loss-of-function phenotypes in a hormone-sensitive background.

These polyclonal knockout cells support diverse applications, including HDAC inhibitor target validation, cohesin acetylation studies, and functional genomics of histone deacetylases. Compatible assays include western blot for histone acetylation, RT-qPCR for gene expression, ChIP-qPCR for histone marks, and functional assays for proliferation, apoptosis, drug sensitivity, and migration/invasion. This tool enables comprehensive investigation of HDAC8 in breast cancer and preclinical drug testing. For further information, contact Ascent Research.

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