The DNMBP Knockout HGC-27 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population in which the DNMBP gene has been disrupted via CRISPR/Cas9-mediated gene targeting. This polyclonal population, derived from the HGC-27 human gastric carcinoma cell line, provides a heterogeneous loss-of-function model for investigating the biological roles of DNMBP in gastric cancer biology. The knockout model enables the study of DNMBP-dependent signaling, cytoskeletal dynamics, and membrane trafficking without the influence of clonal variation, making it suitable for population-level functional assays.
The HGC-27 cell line was originally established from a lymph node metastasis of an undifferentiated gastric carcinoma, and it is widely employed as a model for gastric cancer invasion, proliferation, and metastatic dissemination. As an epithelial adenocarcinoma cell line of human origin, HGC-27 expresses characteristic markers of gastric epithelium and retains key signaling pathways involved in cell adhesion, migration, and tumor progression. This aggressive cancer model is particularly valuable for elucidating mechanisms of lymph node metastasis and for evaluating therapeutic interventions targeting metastatic processes.
DNMBP (Dynamin Binding Protein) functions as a scaffold protein and a guanine nucleotide exchange factor (GEF) for the Rho-family GTPase Cdc42. It integrates signals from integrin-mediated adhesion and receptor tyrosine kinases to orchestrate actin cytoskeleton remodeling, cell junction assembly, and endocytosis. Mechanistically, DNMBP interacts with dynamin, cortactin, WASP, and N-WASP, and it promotes Cdc42-GTP loading, leading to activation of downstream effectors such as the Arp2/3 complex and actin polymerization. Through these interactions, DNMBP plays a critical role in the formation and stabilization of adherens and tight junctions by regulating proteins like ZO-1 and occludin, thereby controlling cell polarity and barrier function.
In the context of HGC-27 gastric cancer cells, disruption of DNMBP is expected to impair Cdc42 activation, resulting in defective actin dynamics and compromised cell-cell adhesion. This loss of function disrupts tight junction integrity and endocytic trafficking, ultimately attenuating cell migration and invasive capacity. The DNMBP knockout polyclonal HGC-27 population therefore serves as a relevant model to dissect the molecular underpinnings of gastric cancer metastasis, allowing researchers to examine how DNMBP-dependent Cdc42 signaling influences tumor cell dissemination and lymph node colonization.
This polyclonal knockout model is ideally suited for a range of advanced research applications, including the investigation of gastric cancer metastasis mechanisms, the study of tight junction and cell polarity regulation, and drug target validation for DNMBP-associated cancers. It can be used in assays such as Western blotting for DNMBP and Cdc42-GTP levels, immunofluorescence localization of ZO-1 and occludin, wound healing migration assays, transwell invasion assays, pull-down of active Cdc42, and co-immunoprecipitation of DNMBP binding partners. Additionally, the model supports screening for pharmacological modulators of actin dynamics and Cdc42 signaling. For further information or technical support, please contact Ascent Research.
