The GOLGA2 Knockout CAL-27 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal human cell population engineered to disrupt the GOLGA2 gene, which encodes the cis-Golgi matrix protein GM130. This polyclonal knockout model provides a heterogeneous pool of cells with targeted loss-of-function mutations in GOLGA2, enabling robust investigation of Golgi structure-function relationships without clonal selection. The product is delivered as a polyclonal population, offering a versatile tool for functional genomics studies in oral cancer research. As a CRISPR/Cas9-mediated gene disruption model, it allows researchers to dissect the roles of GOLGA2 in cellular processes such as vesicle tethering, Golgi ribbon maintenance, and mitotic Golgi dynamics.
The knockout was generated in the CAL-27 cell line, a widely used human tongue squamous cell carcinoma model derived from a tongue epithelial tumor. CAL-27 cells exhibit characteristic features of oral cancer, including anchorage-independent growth and invasive potential, making them a relevant system for studying tumor progression and metastasis. This host cell line retains key signaling pathways associated with head and neck squamous cell carcinoma, providing a physiologically relevant background for investigating Golgi-mediated mechanisms in cancer.
GOLGA2 encodes GM130, a core component of the cis-Golgi matrix that orchestrates Golgi ribbon formation through its interaction with GRASP65 (GORASP1) and facilitates COPI vesicle tethering via the vesicle docking protein p115 (USO1). GM130 acts downstream of the small GTPase ARF1 and is regulated by cell cycle kinases CDK1 and PLK1, which phosphorylate the protein to drive mitotic Golgi disassembly and reassembly. The protein also interacts with ZFPL1, RAB1, TRIP11/GMAP-210, and AKAP450, forming a network that coordinates Golgi organization, vesicle-mediated transport, and cell polarity. Dysregulation of GOLGA2 is implicated in enhanced cell migration and invasion, linking Golgi structural integrity to epithelial tumor progression.
In the context of CAL-27 oral cancer cells, GOLGA2 knockout disrupts the normal Golgi ribbon architecture, potentially altering protein secretion, cell polarity, and migratory behavior. This model is particularly valuable for dissecting how Golgi fragmentation contributes to the aggressive phenotype of tongue squamous cell carcinoma. By comparing GOLGA2-disrupted polyclonal cells with wild-type CAL-27, researchers can assess changes in Golgi morphology, vesicular trafficking, and downstream signaling effects on tumor cell dynamics. The polyclonal nature of the knockout population also allows for the study of heterogeneous gene-disruption outcomes within an epithelial tumor context.
This GOLGA2 knockout model is suitable for a broad range of functional assays, including immunofluorescence to visualize Golgi structure, western blotting for protein expression analysis, and cell migration/invasion assays to evaluate metastatic potential. It also supports secretion assays, proliferation studies, drug sensitivity screening, and transcriptomic analyses such as RT-qPCR and RNA-seq. Flow cytometry can be employed to assess cell cycle progression or apoptotic responses related to Golgi stress. For additional details or technical support, please contact Ascent Research.
