The GOLGA2 Knockout 143B Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout population of human 143B osteosarcoma cells, engineered to disrupt the GOLGA2 gene encoding the cis-Golgi matrix protein GM130. This polyclonal knockout product offers a heterogeneous pool of edited cells, providing a robust loss-of-function model for studying Golgi apparatus dynamics and associated cellular processes without clonal selection biases. The CRISPR/Cas9-mediated gene disruption ablates GM130 expression, enabling researchers to dissect its essential roles in maintaining Golgi structural integrity, regulating vesicle tethering, and coordinating mitotic Golgi fragmentation.
The parental 143B cell line is a widely used human osteosarcoma model derived from the TE85 lineage, characterized by its neoplastic osteoblast-like phenotype, high tumorigenicity, and pronounced metastatic capacity. These cells retain expression of osteoblastic markers, making them particularly suitable for investigating bone cancer biology, bone metastasis mechanisms, and osteoblast-related signaling pathways. The 143B background provides a relevant context for examining how GOLGA2 dysfunction influences cancer cell behavior, including migration, invasion, and tumor progression.
GM130, encoded by GOLGA2, functions as a critical cis-Golgi matrix scaffold that tethers transport vesicles through direct interactions with USO1/p115 and the GRASP65/GORASP1 protein. It is regulated by mitotic kinases CDK1 and PLK1, which phosphorylate GM130 to drive Golgi disassembly during cell division. Downstream, GM130 coordinates integrin trafficking and autophagic flux, as evidenced by altered LC3 and p62 levels upon its depletion. Additionally, GM130 interacts with RAB1, ARF1, STX5, and AKAP450, linking Golgi organization to ER-to-Golgi transport, glycan biosynthesis, and cytoskeletal dynamics.
In the 143B osteosarcoma model, GM130 knockout allows dissection of Golgi-dependent mechanisms that drive cancer cell migration, invasion, and metastasis, as GM130 is known to influence integrin recycling and cell adhesion. Because 143B cells exhibit high metastatic potential, this knockout product is particularly valuable for assessing how Golgi structural disruption impacts tumor cell dissemination and for identifying Golgi-targeted therapeutic vulnerabilities. Furthermore, the model enables exploration of crosstalk between Golgi fragmentation and autophagy in a neoplastic background, given the reported links to LC3 and p62 pathways.
Researchers can utilize these GOLGA2 knockout 143B polyclonal cells for a broad range of experimental applications, including high-resolution immunofluorescence microscopy to assess Golgi morphology changes, Western blotting for GM130 and autophagy markers (LC3, p62), and Transwell assays to quantify migration and invasion deficits. The model supports phosphoproteomic and RNA-seq analyses to map altered signaling networks, as well as co-immunoprecipitation studies to validate GM130 interactions with USO1/p115, GORASP1, and other partners. High-throughput drug screening for Golgi-disrupting agents and investigations into mitotic Golgi disassembly using synchronized cell populations are also facilitated. For further details and technical specifications, please contact Ascent Research.
