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Cat. No. ARG43882

GOLGA8B Knockout SW620 Cell Line

  • Product Type:

    In Stock Cell Lines

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Large intestine (colon)

  • Disease:

    Adenocarcinoma

The GOLGA8B Knockout SW620 Cell Line is a CRISPR/Cas9-edited knockout cell line targeting GOLGA8B in the SW620 human colorectal adenocarcinoma model. GOLGA8B is a cis-Golgi golgin that tethers vesicles to the Golgi, interacting with ARF1, Rab1, GM130, and GOLGA2 to organize COPI/COPII trafficking and the secretory pathway. Knockout disrupts these processes, offering a tool to study Golgi biology and metastatic mechanisms. Derived from a lymph node metastasis, SW620 cells exhibit high invasive potential, making this knockout line ideal for investigating how Golgi-dependent secretion influences cancer cell migration, invasion, and matrix remodeling. Applications include western blotting, immunofluorescence, electron microscopy, and functional assays for drug screening and pathway analysis.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    SW620

    Sex of Donor

    Male

    Age

    51 years

    Gene Name

    GOLGA8B

    Gene Identifier

    NCBI Gene ID 440270

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    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 GOLGA8B Knockout SW620 Cell Line is a CRISPR/Cas9-edited knockout cell line designed to disrupt the GOLGA8B gene in the human SW620 colorectal adenocarcinoma cell line. This knockout model provides a loss-of-function system for investigating the roles of the GOLGA8B golgin in Golgi architecture, vesicle tethering, and secretory pathway dynamics. By using CRISPR/Cas9-mediated gene disruption, researchers can study the consequences of GOLGA8B ablation on cellular trafficking and cancer-related processes.

The SW620 cell line was established from a metastatic lymph node of a 51-year-old Caucasian male with Dukes’ type C colorectal adenocarcinoma. These cells exhibit a highly metastatic phenotype and are widely used as a model for colon cancer metastasis. The SW620 background offers a relevant context for examining how Golgi-associated proteins contribute to malignant progression, given the line’s established invasive properties and its origin from a secondary tumor site.

GOLGA8B encodes a cis-Golgi golgin protein that functions in tethering transport vesicles to the Golgi membrane, a critical step for maintaining Golgi stack organization and efficient secretory trafficking. Its activity is regulated by ARF GTPases and Rab GTPases such as ARF1 and Rab1, and it interacts with key Golgi structural components including GM130, GOLGA2, and GRASP65. GOLGA8B participates in organizing COPI and COPII coat-mediated trafficking and influences downstream effectors like Golgi reassembly stacking proteins and cytoskeletal filaments. Through these interactions, GOLGA8B modulates vesicle-mediated transport and the secretory pathway, with potential impacts on cell migration and matrix remodeling.

In the context of colorectal cancer, disruption of GOLGA8B may compromise Golgi morphology and secretory efficiency, potentially impairing processes essential for metastasis such as cell migration, invasion, and extracellular matrix degradation. The SW620 cell line, with its inherent metastatic capacity, provides a physiologically relevant model to dissect the contribution of Golgi-dependent secretion to cancer cell dissemination. This knockout cell line enables researchers to assess how loss of GOLGA8B affects key metastatic behaviors and to identify vulnerabilities in the Golgi-dependent trafficking of pro-invasive factors.

The GOLGA8B Knockout SW620 Cell Line is suited for a range of experimental applications, including immunofluorescence and electron microscopy studies of Golgi architecture, western blotting analysis of Golgi protein expression, and functional assays such as cell migration, invasion, and proliferation. Additionally, this model can be employed in RNA-seq experiments to uncover transcriptional changes linked to GOLGA8B loss, and for drug screening efforts aimed at targeting Golgi dynamics in metastatic cancers. Together, these applications facilitate a deeper understanding of golgin biology and the secretory pathway??s role in cancer progression. For additional details or technical support, please contact Ascent Research.

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