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Cat. No. ARG43936

KIAA0930 Knockout Hela Cell Line

  • Product Type:

    In Stock Cell Lines

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Uterus (cervix)

  • Disease:

    Adenocarcinoma

The KIAA0930 Knockout Hela Cell Line offers a CRISPR/Cas9-edited knockout model in the Hela cervical adenocarcinoma epithelial background. KIAA0930 is implicated in promoting proliferation, migration, and invasion through PI3K/AKT/mTOR signaling, with downstream effects on Cyclin D1 and EMT markers such as N-cadherin. This loss-of-function cell line enables investigation of oncogenic mechanisms and signaling dependencies, supporting applications in drug target validation, EMT research, and tumorigenesis studies using assays like Western blotting, transwell invasion, and xenograft models.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    HeLa

    Sex of Donor

    Female

    Age

    31 years

    Gene Name

    KIAA0930

    Gene Identifier

    NCBI Gene ID 23313

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Temperature

    37°C

    Atmosphere

    5% COâ‚‚

  • 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. It 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 KIAA0930 Knockout Hela Cell Line is a CRISPR/Cas9-edited knockout cell line engineered for targeted disruption of the KIAA0930 gene in Homo sapiens Hela cells. This product provides a stable loss-of-function model in an adherent epithelial host with the knockout introduced by CRISPR/Cas9-mediated gene disruption. The cell line is supplied as a ready-to-use culture, enabling direct integration into functional studies of oncogenic signaling without the need for transient gene silencing, and is suitable for investigating KIAA0930-dependent processes in a malignancy-relevant background.

Hela cells are derived from a human cervical adenocarcinoma and maintain HPV18-positive status, representing a widely employed epithelial cell model in cancer research. Their robust growth characteristics and well-characterized proteome make them particularly suited for studying proliferation, migration, and invasion mechanisms. The epithelial origin of this host cell line provides a physiologically relevant context for dissecting KIAA0930 function, as the gene has been implicated in multiple epithelial malignancies including cervical and breast cancers. Additionally, Hela cells are routinely used for protein expression and signaling pathway analysis, offering a versatile platform for downstream assays.

KIAA0930 functions as a positive regulator of cell proliferation, migration, and invasion, likely through enhancement of the PI3K/AKT/mTOR signaling axis. Mechanistically, the protein is thought to operate downstream of growth factor receptors such as EGFR, leading to activation of AKT and mTOR, which in turn drive cell cycle progression via Cyclin D1 upregulation. Concurrently, KIAA0930 promotes epithelial-mesenchymal transition (EMT), as evidenced by increased expression of mesenchymal markers including N-cadherin and Vimentin. This dual effect on proliferation and motility supports an oncogenic role for KIAA0930, positioning it as a potential node in signaling networks that coordinate tumor growth and metastasis.

Disruption of KIAA0930 in the Hela background provides a direct approach to evaluate its contribution to oncogenic signaling in an epithelial carcinoma model. Researchers can assess how loss of KIAA0930 alters AKT phosphorylation, mTOR activity, and EMT marker profiles, thereby clarifying the gene’s role in maintaining transformed phenotypes. This model is particularly valuable for comparing signaling dependencies between wild-type and knockout counterparts, enabling dissection of KIAA0930-specific effects on cell cycle regulation and invasive capacity within a well-defined genetic context.

This knockout cell line supports a broad range of applications in cancer biology and drug discovery. Typical experimental workflows include Western blotting to quantify phospho-AKT and EMT protein levels, colony formation assays to measure clonogenic survival, transwell migration and invasion assays to assess motility, CCK-8 viability assays for proliferation, and flow cytometric cell cycle analysis. Additionally, the line can be employed in xenograft tumor models to evaluate in vivo tumorigenesis. For further information about validation and culture conditions, please contact Ascent Research.

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