The DPYSL2 Knockout HGC-27 Polyclonal Cells product comprises a polyclonal population of HGC-27 human gastric carcinoma epithelial cells in which the DPYSL2 gene has been disrupted via CRISPR/Cas9-mediated gene targeting. This polyclonal format provides a heterogeneous knockout pool suitable for functional studies without clonal selection bias.
HGC-27 is a human gastric carcinoma cell line originally derived from a metastatic lymph node; it displays epithelial morphology and serves as a well-established model for investigating gastric cancer progression, invasion, and metastasis. The cells retain key oncogenic features and are widely employed to study tumor cell motility, extracellular matrix remodeling, and signal transduction mechanisms driving aggressive gastric cancer phenotypes.
DPYSL2 encodes collapsin response mediator protein 2 (CRMP2), a phosphoprotein that integrates multiple upstream signals to control cytoskeletal dynamics. CRMP2 is activated downstream of Sema3A/neuropilin-1/plexin-A1 complexes and undergoes regulatory phosphorylation by kinases including Cdk5 and GSK-3??. It interacts directly with tubulin, actin, and vimentin, modulates WAVE1 complex activity, and influences Rho GTPase signaling through Rac1 and RhoA. In concert with effectors such as PAK, LIMK, and cofilin, CRMP2 governs actin depolymerization, microtubule polymerization, lamellipodia formation, and cell migration. Its signaling network intersects with PI3K/Akt and MAPK/ERK pathways, and it has been implicated in the regulation of E-cadherin expression and epithelial-mesenchymal plasticity.
In HGC-27 gastric cancer cells, disruption of DPYSL2 is anticipated to impair CRMP2-dependent cytoskeletal remodeling, thereby attenuating semaphorin-induced actin dynamics and reducing migratory and invasive capacity. This knockout model provides a relevant platform to dissect the contribution of CRMP2 to gastric carcinoma aggressiveness, particularly its role in mediating pro-invasive signals from the tumor microenvironment. By abolishing DPYSL2 expression, researchers can probe the resulting alterations in Rho GTPase activation, PI3K/Akt pathway activity, and downstream effectors that control gastric cancer cell dissemination.
Typical research applications include investigating the role of DPYSL2 in gastric cancer invasion and metastasis, screening for small molecules that target CRMP2-mediated migration, and studying semaphorin signaling in gastrointestinal tumors. The knockout cells are compatible with assays such as Western blotting for CRMP2 and its phosphorylated forms, transwell migration and invasion assays, immunofluorescence staining of actin and tubulin, RT-qPCR for DPYSL2 and related genes, Rho GTPase activation assays, wound healing assays, and live-cell imaging of cytoskeletal dynamics. For additional information or assistance with experimental design, please contact Ascent Research.
