The DPYSL2 Knockout A2780 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout population of the A2780 human ovarian carcinoma cell line with targeted disruption of the DPYSL2 gene. This knockout model provides a loss-of-function system to dissect the cellular roles of DPYSL2-encoded collapsin response mediator protein 2 (CRMP2) without introducing monoclonal artifacts. The polyclonal format ensures representation of diverse editing events across the population, offering a robust tool for studying gene function in a near-native cellular context.
A2780 is a widely employed epithelial ovarian cancer cell line established from a treatment-na?ve patient tumor. It serves as a foundational model for investigating ovarian cancer biology, including signaling pathways that drive proliferation, migration, and chemoresistance. A2780 cells retain key characteristics of high-grade serous ovarian carcinoma and are routinely used to evaluate sensitivity to platinum-based agents such as cisplatin, making them ideal for dissecting mechanisms of drug resistance.
DPYSL2 encodes CRMP2, a cytosolic phosphoprotein that mediates semaphorin-3A (Sema3A) signaling and cytoskeletal reorganization. When Sema3A binds neuropilin-1/plexinA1, kinases Fyn, CDK5, and GSK3?? phosphorylate CRMP2 at sites like Thr514, altering its affinity for tubulin and actin regulators. This phosphorylation cascade modulates microtubule polymerization and actin dynamics, directing cell migration and axon guidance. CRMP2 interacts with ROCK1/2, connecting semaphorin signaling to RhoA-driven cytoskeletal contraction, and associates with LKB1 and Numb, implicating mTOR and Wnt pathway crosstalk.
In ovarian carcinoma, CRMP2 has been linked to tumor cell migration, invasion, and resistance to cisplatin. A2780 cells lacking functional CRMP2 via polyclonal knockout allow researchers to directly assess how loss of this microtubule regulator affects epithelial-to-mesenchymal transition-like phenotypes, focal adhesion turnover, and chemosensitivity. Because CRMP2 is phosphorylated downstream of multiple oncogenic inputs, this model enables systematic dissection of pathway contributions to ovarian cancer aggressiveness without relying on chemical inhibitors that may have off-target effects.
This knockout product is suited for a broad range of functional assays. Western blotting with phospho-specific antibodies (e.g., anti-phospho-T514 CRMP2) confirms target disruption and assesses kinase feedback. Transwell and tubulin polymerization assays measure motility and microtubule stability. MTT and cisplatin sensitivity assays quantify chemoresistance. Immunofluorescence visualizes microtubule reorganization. This polyclonal knockout population is a valuable tool for dissecting semaphorin signaling, cytoskeletal dynamics, and ovarian cancer chemoresistance. For further details, contact Ascent Research.
