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Cat. No. ARG35863

HDAC6 Knockout CAL27 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Oral cavity (tongue)

  • Disease:

    Adenosquamous carcinoma

HDAC6 Knockout CAL-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the human tongue squamous cell carcinoma cell line CAL-27. This model disrupts the HDAC6 gene encoding a cytoplasmic deacetylase that targets ??-tubulin and Hsp90, regulating cell migration, aggresome formation, and protein homeostasis. The knockout cells enable head and neck cancer research by altering stress responses and motility, providing a platform to study drug resistance and tumor invasion. Applications include HDAC inhibitor screening, cell migration assays, and autophagy research, with molecular readouts such as acetylated ??-tubulin levels and aggresome immunofluorescence. The polyclonal format preserves population heterogeneity for robust functional studies.

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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

    HDAC6

    Gene Identifier

    NCBI Gene ID 10013

    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

The HDAC6 Knockout CAL-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human CAL-27 cell line, designed for loss-of-function studies of HDAC6. The polyclonal format provides a heterogeneous pool of genetically disrupted cells, avoiding clonal selection bias and preserving population diversity for robust functional analyses.

CAL-27 is an adherent epithelial cell line derived from a tongue squamous cell carcinoma of a 56-year-old male. These HPV-negative, p53 wild-type cells are widely used to model head and neck cancer, exhibiting characteristic features of epithelial adhesion, migration, and in vivo tumorigenicity.

HDAC6 is a cytoplasmic deacetylase that primarily targets acetylated ??-tubulin and Hsp90, regulating microtubule dynamics, cell migration, and protein chaperone function. Its activity is responsive to upstream stimuli including EGF, TGF-??, and oxidative stress, and it feeds into signaling pathways such as NF-??B (via IKK??/?? and p65), Ras (via RhoA, Rac1, Cdc42), and FoxO. HDAC6 interacts with p97/VCP, ubiquitin, PP1, and survivin, and it controls downstream effectors like cortactin, peroxiredoxins, FoxO1/3, and tau protein. CRISPR/Cas9-mediated gene disruption in CAL-27 cells generates a loss-of-function model that profoundly alters these interconnected networks.

In the CAL-27 background, HDAC6 knockout disrupts aggresome formation and autophagy flux, sensitizing cells to proteotoxic and genotoxic stress and highlighting the enzyme??s role in tumor cell stress adaptation. Additionally, loss of HDAC6 impairs microtubule acetylation-dependent cell migration and adhesion, providing a physiologically relevant model to study invasive potential and therapeutic vulnerabilities in head and neck squamous cell carcinoma.

Researchers can employ these polyclonal knockout cells in a variety of assays, including western blotting for acetylated ??-tubulin and Hsp90 acetylation, cell migration and invasion assays, HDAC activity measurements, and flow cytometry-based apoptosis detection. Immunofluorescence can visualize aggresome formation, and qRT-PCR can quantify HDAC6 target gene expression. These applications make the model suitable for cancer biology, drug resistance research, HDAC inhibitor screening, and neurodegeneration studies. For further details, please contact Ascent Research.

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