The DNM1 knockout HGC-27 polyclonal cells are a CRISPR/Cas9-edited human gastric adenocarcinoma cell population engineered to disrupt the DNM1 gene. This polyclonal knockout model provides a heterogeneous pool of gene-edited cells that closely reflects the genetic diversity of tumor cell populations, facilitating the study of dynamin-1 in endocytosis and cancer biology without the artifacts of clonal selection.
The parental HGC-27 line was derived from a metastatic lymph node of a gastric adenocarcinoma and retains epithelial morphology. It is a widely recognized model for investigating the molecular mechanisms driving gastric cancer metastasis and tumor progression, due to its invasive properties and relevance to advanced disease.
Dynamin-1, encoded by DNM1, is a mechanochemical GTPase that functions as the key scission protein in clathrin-mediated endocytosis (CME). Upon activation by upstream signals including receptor tyrosine kinases such as EGFR, Src kinases, PIP2, and GTP, dynamin-1 oligomerizes at the necks of invaginated clathrin-coated pits. It interacts with clathrin, the AP-2 complex, endophilin A, amphiphysin, cortactin, and SNX9 to assemble the endocytic machinery. GTP hydrolysis then drives membrane constriction and vesicle release. This process regulates receptor internalization and the recycling of integrins from endosomes, thereby controlling focal adhesion disassembly and cell migration.
In HGC-27 gastric cancer cells, disruption of DNM1 profoundly attenuates CME, impairing integrin trafficking and focal adhesion turnover. Consequently, cells exhibit reduced migratory and invasive capacities, underscoring the essential role of dynamin-1 in metastatic behavior. This knockout model thus provides a powerful tool to dissect the contribution of endocytic pathways to gastric cancer progression and to evaluate anti-metastatic strategies.
Researchers can apply this product in a variety of experimental settings, including transferrin uptake assays to monitor CME, wound healing and Matrigel invasion assays to quantify migration and invasion, and co-immunoprecipitation or immunofluorescence to study protein interactions. It is also suitable for drug sensitivity screening and transcriptomic analyses (e.g., RNA-seq) to explore dynamin-1-dependent gene expression changes. For additional details or technical support, please contact Ascent Research.
