The DUS3L Knockout Huh-7 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for functional studies of the DUS3L gene in human hepatocellular carcinoma. This product utilizes CRISPR/Cas9-mediated gene disruption to silence DUS3L expression in the Huh-7 host cell line, providing a heterogeneous pool of cells with targeted inactivation of the dihydrouridine synthase DUS3L. The polyclonal format ensures representation of a broad range of editing events while maintaining the native cellular context of liver cancer.
The Huh-7 cell line, derived from a 57-year-old Japanese male with hepatocellular carcinoma, exhibits adherent epithelial morphology and retains key characteristics of malignant hepatocytes. As a parenchymal liver cell model, Huh-7 is permissive to hepatitis C virus replication and is widely used in liver cancer research, including studies of hepatocarcinogenesis, drug metabolism, and viral oncology. This well-characterized line provides a physiologically relevant background for investigating DUS3L function in hepatic tumor biology.
DUS3L encodes a predicted dihydrouridine synthase that catalyzes the reduction of uridine to dihydrouridine at specific positions in the D-loop of tRNA molecules. This post-transcriptional modification is critical for tRNA stability and translation fidelity. DUS3L likely functions within RNA modification complexes, interacting with tRNA substrates and components of the translation machinery. Downstream, DUS3L-mediated modification influences ribosome function and translation elongation efficiency. Although its upstream regulators remain poorly defined, transcriptional control probably governs DUS3L expression. By modulating dihydrouridine levels, DUS3L connects tRNA metabolism to translational control and RNA metabolic pathways.
In the context of hepatocellular carcinoma, DUS3L disruption may alter tRNA modification patterns, leading to aberrant protein synthesis and potentially contributing to malignant phenotypes. Huh-7 cells, as a model of liver cancer, enable investigation of how DUS3L loss affects translation-dependent processes such as proliferation, colony formation, and stress responses. This knockout model allows researchers to dissect the role of tRNA modifications in hepatocarcinogenesis and to evaluate DUS3L as a candidate for therapeutic intervention in liver cancer.
This polyclonal knockout cell population is suitable for a variety of functional assays. Western blotting and RT-qPCR confirm DUS3L knockout efficiency, while LC-MS/MS can directly measure changes in dihydrouridine modification of tRNA. Puromycin incorporation assays assess global translation rates, and cell proliferation or colony formation assays evaluate the impact on tumor cell growth. These cells enable detailed mechanistic studies on how DUS3L-dependent tRNA modification influences protein synthesis in hepatocellular carcinoma, facilitating the identification of downstream targets and interacting partners. For additional information or to place an order, please contact Ascent Research.
