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Cat. No. ARG35394

IFT88 Knockout CAL27 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Oral cavity (tongue)

  • Disease:

    Adenosquamous carcinoma

The IFT88 Knockout CAL-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population targeting IFT88 in the oral squamous cell carcinoma line CAL-27. IFT88 is a core intraflagellar transport-B (IFT-B) protein essential for primary cilium assembly, and its disruption impairs ciliary-dependent Sonic hedgehog (Shh) signaling via GLI transcription factors, PDGFR??-mediated AKT and ERK activation, and Wnt pathways. This model enables investigation of ciliary roles in oral cancer tumorigenesis, ciliopathy research, and drug target validation. Key assays include immunofluorescence for acetylated tubulin, Shh reporter, migration/invasion, and apoptosis analyses, providing a versatile platform for cilia and cancer studies.

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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

    IFT88

    Gene Identifier

    NCBI Gene ID 8100

    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 IFT88 Knockout CAL-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the human oral squamous cell carcinoma line CAL-27. This product offers a targeted disruption of the IFT88 gene, enabling loss-of-function studies of intraflagellar transport complex B (IFT-B) function. The polyclonal format provides a heterogeneous knockout pool, minimizing clonal artifacts and facilitating robust phenotypic analyses.

CAL-27 is a well-characterized epithelial cell line derived from a tongue squamous cell carcinoma. Its tumorigenic properties and retaining of functional primary cilia make it an ideal host for investigating ciliary biology in a cancer context. This model recapitulates the molecular landscape of oral cancer, allowing dissection of cilium-dependent and -independent mechanisms in tumor progression.

IFT88 encodes a core component of the IFT-B complex, essential for anterograde transport and primary cilium assembly. Its knockout abrogates ciliogenesis and disrupts ciliary signaling. Upstream regulators include RFX2, RFX3, and FOXJ1. IFT88 deficiency impairs Sonic hedgehog (Shh) pathway transduction, attenuating GLI1, GLI2, and GLI3 activity. It also diminishes PDGFR?? signaling, reducing downstream AKT and ERK1/2 phosphorylation. IFT88 directly interacts with IFT20, IFT52, IFT57, IFT81, kinesin-2, and dynein-2 to form the IFT-B holocomplex. Loss of IFT88 therefore compromises cilium-dependent Shh, Wnt, and PDGFR?? pathways.

In oral squamous cell carcinoma, primary cilium status is increasingly recognized as a modulator of cell behavior. The IFT88 knockout in CAL-27 cells provides a precise genetic tool to evaluate how cilium removal impacts tumor cell proliferation, migration, and drug responses. By uncoupling ciliary and non-ciliary signaling, this model helps clarify the significance of Shh and PDGFR?? pathways in cancer, contributing to the identification of novel therapeutic targets.

These polyclonal knockout cells are suited for studies of primary cilia in cancer biology, ciliopathy modeling, and drug target validation. Typical experimental applications include immunofluorescence staining for acetylated tubulin or ARL13B to confirm cilium loss, Western blot and RT-qPCR for IFT88 depletion, RNA-seq for transcriptomic profiling, flow cytometry for cell cycle, and functional assays such as migration, invasion, and drug sensitivity. Hedgehog pathway reporter and apoptosis assays extend the model’s utility. For further assistance, contact Ascent Research.

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