The EDEM2 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting EDEM2 in the HGC-27 human gastric cancer cell line. This gene-disruption model offers a stable loss-of-function system for studying endoplasmic reticulum-associated degradation (ERAD). The polyclonal knockout cells enable functional analyses without single-cell cloning, providing a versatile tool for investigating EDEM2-dependent processes in a gastric adenocarcinoma background.
HGC-27 cells were established from the metastatic lymph node of an undifferentiated gastric adenocarcinoma patient. They retain aggressive features such as rapid proliferation and metastatic potential, making them a relevant model for gastric cancer research. The epithelial origin and tumorigenic properties of HGC-27 allow mechanistic exploration of ER stress responses and protein quality control in malignancy.
EDEM2 is an ER-resident lectin that recognizes mannose-trimmed N-glycans on misfolded glycoproteins, targeting them for retrotranslocation and proteasomal degradation via the HRD1-SEL1L ERAD complex. It interacts with OS9, DERL1, and VIMP to facilitate substrate clearance. EDEM2 expression is upregulated by the unfolded protein response (UPR) through ATF6, XBP1, and the PERK/eIF2??/ATF4 pathway. By alleviating ER stress, EDEM2 promotes cell survival, integrating glycoprotein quality control with cellular homeostasis.
In gastric cancer, heightened ER stress necessitates robust ERAD activity for survival. Disrupting EDEM2 in HGC-27 cells enables dissection of how impaired glycoprotein degradation affects cancer cell viability, metastasis, and drug resistance. The metastatic origin of HGC-27 makes this model especially valuable for studying EDEM2’s role in lymph node dissemination and adaptation to ER stress. Furthermore, it can be applied to congenital disorders of glycosylation and neurodegenerative disease mechanisms.
Applications include knockout validation by western blotting and RT-qPCR, monitoring of ER stress markers via flow cytometry, and apoptosis assays under ER stress. Migration and invasion assays, co-immunoprecipitation, and drug sensitivity testing are supported. The model is ideal for screening ERAD-modulating compounds and investigating chemoresistance. For technical inquiries, contact Ascent Research.
