The EDEM2 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A2780 human ovarian adenocarcinoma cell line. This product offers a loss-of-function model for the EDEM2 gene, encoding a key lectin of the endoplasmic reticulum-associated degradation (ERAD) pathway. CRISPR/Cas9-mediated gene disruption enables researchers to examine the consequences of impaired ERAD in a cancer-relevant epithelial background. The polyclonal nature yields a heterogeneous population, suitable for pooled functional analyses without clonal bias.
The A2780 host cell line is a well-characterized human ovarian adenocarcinoma line established from an untreated patient. As an epithelial cell model, A2780 cells retain hallmarks of ovarian cancer, including dysregulated proliferation and chemotherapy sensitivity. The ovarian cancer context is particularly pertinent for studying protein homeostasis, as tumor cells frequently endure proteotoxic stress from rapid growth and metabolic reprogramming. This background is thus ideal for assessing how ERAD disruption influences cancer cell survival and stress adaptation.
EDEM2 functions as a mannose-binding lectin recognizing terminally trimmed ??1,2-mannose residues on misfolded glycoproteins in the ER. This facilitates substrate retrotranslocation by the HRD1-SEL1L complex, followed by ubiquitination and proteasomal degradation. EDEM2 cooperates with EDEM1, EDEM3, OS9, and VCP/p97. Upstream, UPR sensors IRE1 and PERK activate ATF6 and XBP1, which induce EDEM2 expression. Downstream, EDEM2 promotes clearance of substrates such as CD147 and NFE2L1, alleviating ER stress.
In the ovarian cancer setting, EDEM2-mediated ERAD may sustain cell viability by alleviating ER stress triggered by oncogenic signaling and the tumor microenvironment. Loss of EDEM2 in A2780 cells can unmask adaptive vulnerabilities, potentially informing therapeutic strategies. The A2780 line, with its epithelial origin and ovarian cancer background, offers a clinically relevant system to dissect how ERAD dysfunction impacts cancer cell fate, chemoresistance, and metastatic potential. This model enables precise dissection of EDEM2-dependent pathways in ovarian tumor biology.
These polyclonal knockout cells are applicable for diverse functional studies, including analysis of ERAD efficiency via western blotting of EDEM2 and ERAD substrates, monitoring UPR activation with RT-qPCR or immunofluorescence, and assessing cell viability under ER stress conditions. Proteasome activity assays and flow cytometry for apoptosis and cell cycle further extend utility. This product serves as a valuable resource for researchers focused on glycoprotein quality control, ovarian cancer biology, and ER-related diseases. For more information, please contact Ascent Research.
