The DPYSL2 Knockout AGS Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout population of AGS human gastric adenocarcinoma epithelial cells, featuring disruption of the DPYSL2 gene. This loss-of-function model enables precise interrogation of the cellular roles of collapsin response mediator protein 2 (CRMP2), a microtubule-associated protein critical for cytoskeletal organization. The polyclonal format avoids clonal selection artifacts, ensuring a diverse allelic knockout representation for robust functional studies.
The AGS cell line was originally derived from the gastric adenocarcinoma of a 54-year-old female patient and displays an adherent epithelial phenotype. Extensively characterized as a gastric cancer model, AGS cells are routinely employed to study gastric tumorigenesis, including proliferation, migration, invasion, and intracellular signaling. Their genetic stability and well-documented oncogenic properties make them an ideal host for CRISPR-based gene disruption, facilitating the exploration of gene function in a disease-relevant background.
DPYSL2 encodes CRMP2, a cytosolic phosphoprotein coordinating microtubule polymerization and actin reorganization. Its activity is modulated by phosphorylation via GSK3B and CDK5 downstream of SEMA3A/NRP1/PLXNA1 signaling, with additional regulation by RhoA and ROCK. CRMP2 directly interacts with TUBB and ACTB, and forms complexes with FAK and NUMB, linking extracellular cues to cytoskeletal remodeling and controlling cell morphology and motility.
In AGS cells, DPYSL2 knockout impairs CRMP2-driven cytoskeletal control, reducing migration, invasion, and proliferation. This model enables dissection of CRMP2’s contribution to gastric adenocarcinoma aggressiveness and identification of key effectors. By disrupting this pathway, researchers can investigate metastatic mechanisms and therapeutic vulnerabilities in a disease-relevant setting.
This polyclonal knockout product is suited for diverse experimental approaches, including wound healing and Transwell migration assays, Matrigel-based invasion assays, immunofluorescence microscopy of cytoskeletal components (actin and tubulin), in vitro tubulin polymerization assays, and cell viability/proliferation analyses (MTT, BrdU). It also enables drug target validation along the SEMA3A/CRMP2 axis and supports translational studies bridging neurobiology and cancer biology. For additional technical details or customized support, please contact Ascent Research.
