The GOLGA2 Knockout A2780 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal population of A2780 cells harboring targeted disruption of the GOLGA2 gene. This knockout cell product provides a loss-of-function model for investigating the functional role of the GOLGA2-encoded protein, GM130, in cellular processes. The heterogeneous polyclonal format reflects a pool of edited cells with target-gene disruption, enabling robust population-level studies without clonal selection.
The A2780 host cell line is a well-characterized human ovarian carcinoma cell line established from an untreated patient, exhibiting epithelial morphology. As an adherent cell model, A2780 cells are widely employed in epithelial ovarian cancer research, including studies of tumor cell proliferation, metastasis, and chemoresistance. This cellular background is particularly suited for probing the contributions of Golgi-associated proteins to cancer cell phenotypes.
GOLGA2 encodes GM130, a golgin family protein essential for Golgi ribbon integrity and vesicle tethering. Mechanistically, GM130 interacts with GORASP1 (GRASP65) and COPI coatomer components to maintain cisternal stacking. During mitosis, GM130 is phosphorylated by CDK1/Cyclin B and PLK1, leading to Golgi complex disassembly and dispersal. This process is reversed upon dephosphorylation, allowing post-mitotic Golgi reassembly. Upstream regulators include ARF1 GTPase, while downstream effects involve COPI vesicle trafficking and glycosylation enzyme function. Representative pathway components include GOLGA2, GORASP1, COPI, ARF1, CDK1, and PLK1.
In the context of ovarian cancer, disruption of GOLGA2 may compromise Golgi structural organization, potentially altering secretory pathways, glycoprotein processing, and cell cycle progression. The A2780 knockout model thus enables dissection of how GM130-dependent Golgi ribbon maintenance influences ovarian cancer cell behavior, including migration, invasion, and response to platinum-based chemotherapeutics such as cisplatin. Additionally, this model may shed light on the role of Golgi defects in broader cancer-related processes including HPV-associated malignancies and neurodegenerative conditions characterized by Golgi fragmentation.
This polyclonal knockout cell population is suitable for a range of experimental approaches, including immunofluorescence microscopy to assess GM130-positive Golgi morphology, Western blotting for GOLGA2 expression, and co-immunoprecipitation to evaluate interactions with GORASP1 or COPI subunits. Functional assays may include cell viability and apoptosis analyses under chemotherapeutic challenge, migration and invasion assays, Golgi fragmentation assays using lectin staining, and cell cycle distribution analysis. Researchers can employ this model to explore the impact of GOLGA2 loss on intracellular trafficking, mitotic organelle dynamics, and drug resistance mechanisms. For additional details or custom orders, please contact Ascent Research.
