The EDC3 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from the HGC-27 gastric adenocarcinoma cell line, with disruption of the EDC3 gene. This heterogeneous pool of knockout cells is ideal for studying loss-of-function phenotypes in a metastatic gastric cancer model. The polyclonal format captures editing diversity, enabling robust population-level analyses without clonal selection artifacts, and is suitable for investigating the collective impact of EDC3 ablation on mRNA decay pathways and cellular behavior.
The HGC-27 cell line originated from a lymph node metastasis of a gastric adenocarcinoma in a 75-year-old male patient. These cells exhibit an adherent epithelial morphology and are widely utilized as a model for metastatic gastric carcinoma. HGC-27 cells retain key features of gastric cancer, including aggressive growth characteristics and metastatic potential, making them a powerful host for interrogating the role of post-transcriptional regulators in tumor progression and disease biology.
EDC3 encodes a scaffold protein critical for the assembly and function of the mRNA decapping complex. It directly interacts with decapping enzyme DCP2, decapping activator DCP1A, and P-body components DDX6 and EDC4, enhancing DCP2 activity and facilitating 5′-3′ mRNA degradation. EDC3 also associates with the LSM1-7 complex and the CNOT deadenylase complex. Through these interactions, EDC3 promotes P-body formation and regulates the turnover of a broad spectrum of transcripts, including AU-rich element (ARE)-containing mRNAs encoding cytokines and other regulatory proteins.
In HGC-27 cells, EDC3 knockout allows dissection of mRNA decapping contributions to gastric adenocarcinoma pathogenesis. Dysregulation of mRNA decay is linked to cancer, and altered P-body dynamics influence tumorigenesis and stress responses. Disruption of EDC3 scaffold function impairs decapping complex assembly, potentially affecting degradation of oncogenic or tumor-suppressor transcripts. This model enables exploration of how post-transcriptional dysregulation drives gastric cancer cell proliferation, migration, invasion, and malignancy.
Researchers can employ this polyclonal knockout population in a variety of assays, including Western blotting to confirm EDC3 protein depletion, RT-qPCR and RNA-seq to assess changes in mRNA stability and transcriptome profiles, and immunofluorescence to visualize P-body markers such as DCP1A and DDX6. Functional studies may include cell proliferation, migration, and invasion assays to evaluate the phenotypic impact of EDC3 loss in gastric cancer cells. This product is ideally suited for exploring mRNA decay pathways, P-body biology, and post-transcriptional regulatory networks in cancer. For further information, please contact Ascent Research.
