The DUS3L knockout HT29 polyclonal cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HT29 human colorectal adenocarcinoma cell line. This loss-of-function model was generated by CRISPR/Cas9-mediated disruption of DUS3L, eliminating the encoded tRNA-dihydrouridine synthase activity. As a polyclonal population, these cells offer a heterogeneous genetic background for studying DUS3L function without clonal selection bias. They are intended for advanced biomedical research, particularly in tRNA modification and colorectal cancer biology.
The HT29 cell line, established from a primary colorectal adenocarcinoma of a 44-year-old female, serves as a well-characterized model for intestinal epithelial barrier function and colorectal cancer. HT29 cells form polarized monolayers with functional tight junctions, mimicking the intestinal epithelium. This host cell line provides a physiologically relevant environment to study the impact of DUS3L knockout on epithelial biology, including barrier integrity, drug transport, and tumor cell behavior. Its adenocarcinoma origin makes it particularly valuable for investigating connections between tRNA modifications and colorectal carcinogenesis.
DUS3L encodes a tRNA-dihydrouridine synthase that catalyzes the reduction of uridine to dihydrouridine in the tRNA elbow region. This post-transcriptional modification promotes tRNA structural flexibility and influences codon-anticodon interactions, thereby impacting translation efficiency and accuracy. DUS3L directly interacts with its tRNA substrates and may collaborate with other tRNA-modifying enzymes to establish the dihydrouridine modification landscape. Although upstream regulators of DUS3L remain unknown, its activity modulates tRNA stability and protein synthesis dynamics. In the context of colorectal adenocarcinoma, disruption of DUS3L-mediated dihydrouridine modification can alter the cellular translational program, potentially affecting stress responses and tumorigenic properties.
The DUS3L knockout HT29 polyclonal cells enable investigation of how loss of dihydrouridine modification influences intestinal epithelial cell physiology and colorectal cancer cell behavior. Since HT29 cells are a model for barrier function and carcinogenesis, this knockout system allows assessment of DUS3L’s role in maintaining epithelial integrity and its potential contribution to malignant transformation. Researchers can explore whether altered translation dynamics due to DUS3L deficiency impact cellular growth, differentiation, or stress survival, providing insights into the tumorigenic relevance of tRNA modifications.
This polyclonal knockout product is suited for studies integrating tRNA modification profiling and translational analysis in colorectal cancer models. Applications include tRNA sequencing and northern blotting to evaluate dihydrouridine levels, polysome profiling and protein synthesis assays to measure translation changes, and cell viability and barrier integrity assays in the HT29 background. These approaches can dissect DUS3L’s role in colorectal cancer biology and intestinal epithelial function, linking tRNA modification to cellular phenotype. For further details or to request a quote, please contact Ascent Research.
