The EHBP1L1 Knockout HGC-27 Polyclonal Cells product provides a CRISPR/Cas9-mediated gene-disrupted polyclonal cell population derived from the human gastric carcinoma cell line HGC-27. This polyclonal knockout model enables loss-of-function studies of EHBP1L1, a gene encoding an adaptor protein critical for endocytic recycling and actin cytoskeleton organization. By disrupting the target gene across a heterogeneous cell pool, researchers can analyze functional consequences without clonal selection bias, making it suitable for population-level investigations of EHBP1L1-dependent processes in a metastatic cancer context.
The parental HGC-27 cell line originates from a lymph node metastasis of a gastric adenocarcinoma and exhibits an undifferentiated morphology. As a widely used model of metastatic gastric carcinoma, HGC-27 cells retain key oncogenic properties, including migratory and invasive capabilities. This background provides a physiologically relevant system to examine the role of EHBP1L1 in late-stage gastric cancer progression, particularly in pathways governing cell motility and metastatic dissemination.
EHBP1L1 functions as an adaptor linking EH domain-containing proteins EHD1 and EHD2 to the actin cytoskeleton and endocytic machinery. It facilitates recycling endosome trafficking together with Rab11 and Arf6, and promotes actin polymerization via myosin interactions. Signaling downstream of growth factor receptors and Wnt pathway controls its activity, though transcriptional regulation is not fully characterized. Knockout disrupts EHD1/EHD2-mediated recycling and actin dynamics, impairing cell migration. Interactions with actin and other EH domain proteins integrate endosomal trafficking with cytoskeletal remodeling.
In the HGC-27 metastatic gastric cancer context, loss of EHBP1L1 is expected to compromise the efficiency of receptor and adhesion molecule recycling, attenuate actin-driven lamellipodia formation, and reduce invasive capacity. This model thus offers a platform to dissect how aberrations in endocytic recycling contribute to gastric cancer metastasis. It also allows exploration of synthetic lethal interactions or compensatory pathways that may be targeted therapeutically in EHBP1L1-deficient tumors.
Researchers can employ this polyclonal knockout cell population in various experimental settings. Typical applications include transferrin recycling assays to evaluate endocytic trafficking, Transwell migration and invasion assays, and co-immunoprecipitation studies to map EHBP1L1 complexes. Gene expression profiling by RNA-seq or RT-qPCR and proteomics reveal downstream effects. Immunofluorescence visualizes actin reorganization and EHD1/2 distribution. The product suits screening for inhibitors of recycling pathways and validating EHBP1L1 as a therapeutic target. For further details, contact Ascent Research.
