The EIF2D Knockout HGC-27 Polyclonal Cells product provides a ready-to-use CRISPR/Cas9-edited polyclonal knockout cell population derived from the HGC-27 human gastric carcinoma cell line. This pooled format comprises a heterogeneous mix of cells bearing targeted disruption of the EIF2D gene, generated via CRISPR/Cas9-mediated gene editing without single-cell clonal isolation. The polyclonal knockout population retains the diverse genetic background of the parental line while offering a loss-of-function model for functional studies of EIF2D in gastric cancer. Researchers can immediately apply these cells in downstream assays to interrogate the roles of EIF2D in translational control and tumor biology, leveraging the polyclonal nature to mitigate clonal artifacts commonly associated with monoclonal knockout lines.
The host cell line, HGC-27, was established from the metastatic lymph node of a patient with poorly differentiated gastric adenocarcinoma. This cell line serves as a well-characterized in vitro model for gastric cancer research, recapitulating key features of tumor progression and metastasis. Its origin from a metastatic site renders it particularly suitable for investigating molecular mechanisms driving gastric cancer dissemination and for evaluating potential anti-metastatic therapeutic strategies. HGC-27 cells are widely utilized in cancer biology studies, including signal transduction analysis, drug sensitivity testing, and functional genomics, providing a clinically relevant platform for EIF2D knockout experiments.
EIF2D encodes a translation initiation factor that mediates cap-independent protein synthesis by facilitating recruitment of initiator tRNA to the 40S ribosomal subunit, particularly under stress conditions or during selective mRNA translation. EIF2D functions within the broader translational control network, receiving regulatory inputs from mTOR signaling and cellular stress pathways. It interacts physically with key components of the translation machinery, including ribosomes, tRNA, and the eIF2 complex, as well as with ligatin-associated proteins. Downstream, EIF2D modulates global protein synthesis and the translation of specific mRNA subsets, implicating it in the integrated stress response. By influencing translation initiation, EIF2D contributes to the dynamic remodeling of the proteome in response to oncogenic signals, positioning it as a node between nutrient sensing and gene expression in cancer cells.
In the context of HGC-27 gastric carcinoma cells, disruption of EIF2D provides a valuable model to dissect how cap-independent translation contributes to malignant phenotypes. Given the aggressive nature of this poorly differentiated gastric cancer line, EIF2D knockout allows researchers to investigate its role in sustaining proliferation, migration, invasion, and metastatic potential. The model enables functional interrogation of EIF2D-dependent mRNA translation programs that may drive tumor progression and resistance to therapy. Moreover, EIF2D has been proposed as a potential biomarker in gastric cancer, making this knockout tool instrumental for validating its diagnostic or prognostic significance and for exploring synthetic lethal interactions that could reveal new therapeutic vulnerabilities.
Typical experimental applications of the EIF2D Knockout HGC-27 Polyclonal Cells include quantitative analysis of cap-independent translation via polysome profiling, assessment of cellular proliferation, migration, and invasion using standard 2D and 3D assays, and drug sensitivity studies to evaluate the impact of EIF2D loss on chemotherapeutic response. Knockout validation can be performed through western blotting and RT-qPCR to confirm reduced EIF2D protein and mRNA levels, respectively. These cells are also suitable for genome-wide studies such as ribosome profiling or RNA-seq to identify EIF2D-dependent translational targets. For further technical specifications, pricing, or to place an order, please contact Ascent Research.
