The DUS3L Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human gastric adenocarcinoma AGS cell line. This polyclonal pool comprises cells carrying diverse disruptions in the DUS3L gene, providing a robust loss-of-function model for studying tRNA dihydrouridine modification without the influence of single-cell clonal selection.
The AGS cell line is a well-established in vitro model of gastric mucosal epithelium and gastric adenocarcinoma. Exhibiting an adherent epithelial morphology, AGS cells retain key signaling pathways and phenotypic characteristics relevant to gastric carcinogenesis, making them a widely used system in cancer research for investigating tumor cell behavior and drug responses.
DUS3L encodes a dihydrouridine synthase that catalyzes the reduction of uridine to dihydrouridine (D) in tRNA, a modification essential for tRNA structural stability and translational fidelity. DUS3L expression is regulated by the oncogenic transcription factors MYC and HIF1A, and its activity is integrated with the mTORC1 nutrient-sensing pathway. DUS3L interacts with tRNA substrates and components of the tRNA modification enzyme complex, promoting efficient translation of cancer-related mRNAs. Through these molecular interactions, DUS3L functions as a critical node linking tRNA modification to cellular stress adaptation and translational control.
In the gastric adenocarcinoma context, disruption of DUS3L compromises the dihydrouridine modification landscape, leading to impaired translational fidelity and reduced capacity to manage proteotoxic and metabolic stress. This AGS-based knockout model is particularly valuable for dissecting the contribution of tRNA modification fidelity to gastric cancer phenotypes, including proliferation, drug resistance, and metastatic potential. The loss of DUS3L may reveal vulnerabilities in stress-responsive translation pathways that are exploited by cancer cells.
The DUS3L Knockout AGS Polyclonal Cells support a wide range of experimental applications. Researchers can assess DUS3L protein levels by western blotting, quantify tRNA dihydrouridine modifications via LC-MS, and monitor gene expression changes with RT-qPCR. Functional assays such as proliferation, migration/invasion, drug sensitivity, and apoptosis can be performed to evaluate the impact of DUS3L loss on tumor cell behavior. Additionally, ribosome profiling or polysome fractionation can identify mRNAs whose translation is dependent on DUS3L-mediated tRNA modifications, providing deeper insight into translational control in gastric cancer. For additional information or to request a custom quote, please contact Ascent Research.
