The DUS1L Knockout HGC-27 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human gastric carcinoma cell line HGC-27, engineered for targeted disruption of the DUS1L gene. This loss-of-function model utilizes CRISPR/Cas9-mediated gene disruption to eliminate DUS1L expression, providing a valuable tool for investigating the biological consequences of impaired tRNA dihydrouridine modification in a relevant cancer cell context. The polyclonal nature of this knockout population ensures representation of diverse editing events, enabling robust functional studies without clonal selection artifacts.
HGC-27 is an epithelial tumor cell line originally established from the metastatic lymph node of a human gastric adenocarcinoma patient. This cell line retains key characteristics of gastric cancer, including deregulated proliferation, migratory capacity, and activation of oncogenic signaling pathways. As a widely employed model in gastric cancer research, HGC-27 cells are particularly suited for exploring molecular mechanisms underlying tumor progression, metastasis, and therapeutic resistance. The combination of DUS1L knockout with this clinically relevant host cell background creates a physiologically pertinent system for studying tRNA modification biology in the context of gastric malignancy.
DUS1L encodes a dihydrouridine synthase that catalyzes the conversion of uridine to dihydrouridine at defined positions in multiple tRNA species, including tRNA^Leu, tRNA^Ile, and tRNA^Val. This post-transcriptional modification is critical for promoting proper tRNA folding, structural stability, and efficient translation elongation. DUS1L activity is regulated upstream by MYC transcription factor and mTORC1 signaling, linking it to nutrient-sensing and growth-control pathways. The enzyme directly interacts with tRNA substrates and functionally collaborates with other modification factors such as PUS7 and TRMT61A. Downstream, DUS1L-dependent dihydrouridine formation influences ribosome biogenesis and the function of translation elongation factor eEF1A, thereby modulating global protein synthesis and the production of specific oncogenic proteins.
In the gastric carcinoma setting, DUS1L disruption is particularly significant because altered tRNA modification patterns have been implicated in cancer cell adaptation and malignant transformation. DUS1L-mediated dihydrouridine modification supports tRNA stability under conditions of high translational demand, a hallmark of rapidly proliferating tumor cells. By abolishing this activity in HGC-27 cells, the knockout model enables researchers to dissect how loss of tRNA dihydrouridine impacts cellular processes such as proliferation, migration, and metabolic reprogramming that are central to gastric adenocarcinoma progression. Moreover, the model permits investigation of downstream effects on the synthesis of proteins involved in mTOR-driven oncogenic networks.
This polyclonal knockout cell product is ideally suited for a broad range of functional assays, including Western blotting and RT-qPCR for confirming DUS1L disruption, LC-MS-based quantification of tRNA dihydrouridine levels, polysome profiling to evaluate translation dynamics, and puromycin incorporation assays for measuring de novo protein synthesis. In addition, cell-based phenotypic assays such as CCK-8 proliferation and Transwell migration can be employed to link DUS1L activity to gastric cancer cell behavior. These applications facilitate mechanistic studies on translational regulation in cancer, target validation for gastric cancer therapeutics, and exploration of tRNA modification defects in related disorders. For further information and custom solutions, please contact Ascent Research.
