The EIF5A2 Knockout HGC-27 Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal population in which the EIF5A2 gene has been disrupted across a heterogeneous pool of HGC-27 gastric carcinoma cells. This format avoids the selection biases of monoclonal isolation, preserving a spectrum of editing outcomes that collectively represent the functional consequences of EIF5A2 loss. The product provides a robust and biologically relevant model for studying EIF5A2-dependent processes without the limitations of single-cell-derived clones. It is designed for advanced applications in cancer biology and translational research.
The parental HGC-27 cell line was established from a lymph node metastasis of a gastric adenocarcinoma, representing an aggressive and metastatic epithelial model of gastric cancer. These cells display invasive properties, deregulated proliferation, and resistance to anoikis, key hallmarks of advanced disease. Widely used in metastasis and EMT research, HGC-27 provides a clinically relevant background for dissecting the molecular drivers of tumor dissemination. Knocking out EIF5A2 in this context enables precise evaluation of its contribution to the malignant phenotype of metastatic gastric carcinoma.
EIF5A2 encodes a specialized translation elongation factor that undergoes hypusination??a unique post-translational modification essential for its activity. The hypusine moiety is formed by the sequential action of deoxyhypusine synthase (DHPS) and deoxyhypusine hydroxylase (DOHH). Once activated, EIF5A2 binds the ribosomal large subunit to facilitate translation of mRNAs encoding polyproline stretches, including cyclin D1 (CCND1), vimentin (VIM), ??-catenin (CTNNB1), and the EMT inducer Snail (SNAI1). Transcriptionally, EIF5A2 is a target of the MYC oncoprotein and responds to EGF signaling, integrating translational control with mTOR and MYC-driven pathways to promote cell cycle progression and epithelial-mesenchymal transition.
In HGC-27 cells, EIF5A2 serves as a critical link between translational output and the aggressive biology of metastatic gastric cancer. Its disruption is expected to downregulate synthesis of key oncogenic proteins such as cyclin D1 and vimentin, leading to impaired cell cycle progression and reduced invasive capacity. This knockout model allows researchers to disentangle translation-specific contributions from broader transcriptional programs, offering insight into how EIF5A2 sustains malignancy. It provides a unique tool for probing the vulnerability of translation-dependent oncogenic signaling in a clinically relevant gastric cancer context.
Routine applications include Western blotting for EIF5A2, cyclin D1, and vimentin; RT-qPCR for transcript analysis; MTT proliferation assays; transwell migration/invasion assays; and cell cycle flow cytometry. Detection of hypusinated EIF5A2 provides a direct measure of its active state. These cells support investigations of gastric cancer invasion mechanisms, validation of EIF5A2-targeted therapies, and dissection of translation-controlled oncogenic networks. For additional product details and technical support, please contact Ascent Research.
