The DPYSL5 Knockout HGC-27 Polyclonal Cells product consists of a CRISPR/Cas9-edited polyclonal population of HGC-27 human gastric carcinoma cells with targeted disruption of the DPYSL5 gene. This polyclonal knockout pool is generated by transient delivery of CRISPR/Cas9 components, yielding a heterogeneous collection of cells with diverse loss-of-function mutations. The non-clonal format avoids single-cell cloning biases while providing a ready-to-use model for functional studies. Cells are provided cryopreserved and validated for DPYSL5 gene disruption.
HGC-27 is a gastric carcinoma cell line isolated from a lymph node metastasis of a gastric adenocarcinoma. It displays epithelial morphology and is tumorigenic, serving as a widely used model for gastric cancer metastasis, invasion, and EMT research. Its robust growth and amenability to genetic manipulation make it an ideal host for knockout studies aimed at deciphering molecular mechanisms of tumor progression.
DPYSL5 (CRMP5) is a microtubule- and actin-binding protein that regulates cytoskeletal dynamics downstream of semaphorin?Cneuropilin signaling. Activated by Sema3A through the Neuropilin-1/Plexin-A receptor complex, CRMP5 interacts directly with tubulin and actin to control polymerization and filament organization. It is also modulated by neurotrophins (BDNF, NGF) and growth factors (EGF, FGF, Wnt ligands), integrating inputs into MAPK/ERK and PI3K/AKT pathways. Downstream targets include Cyclin D1, E-cadherin, and Vimentin, linking CRMP5 to cell proliferation and EMT. CRMP5 complexes with other CRMP family members (DPYSL2, DPYSL3) and kinesin to mediate microtubule-based transport and RhoA/ROCK/FAK-dependent migration. In cancer, DPYSL5 promotes invasion by driving cytoskeletal reorganization and EMT.
In HGC-27 cells, DPYSL5 knockout enables dissection of its role in gastric cancer metastasis. As HGC-27 originates from a metastatic site, the polyclonal knockout cells are well suited for studying effects on cell migration, invasion, and EMT marker expression. Disruption of DPYSL5 may perturb cytoskeletal remodeling downstream of Sema3A/neuropilin and alter proliferative signaling via MAPK/ERK and PI3K/AKT, providing insights into CRMP5??s contribution to gastric cancer progression.
These cells support diverse applications including Transwell invasion/migration assays, Western blotting, RT-qPCR, and immunofluorescence for cytoskeletal and EMT markers. Co-immunoprecipitation can be used to probe interactions with tubulin, actin, and Plexin-A. Cell proliferation (MTT) and drug screening assays help evaluate DPYSL5??s role in tumor growth and therapeutic responses. For additional information, please contact Ascent Research.
