The DYNLT3 Knockout Huh-7 Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Huh-7 human hepatocellular carcinoma cell line, targeting the DYNLT3 gene via CRISPR/Cas9-mediated gene disruption. This polyclonal product format provides a heterogeneous pool of knockout cells, enabling robust loss-of-function studies without clonal isolation. The disruption of DYNLT3, encoding a dynein light chain subunit, offers a powerful tool to investigate dynein motor complex functions in a hepatocarcinoma context.
The Huh-7 parental cell line originates from a well-differentiated hepatocellular carcinoma of a 57-year-old male patient. It retains many hepatocyte-like characteristics, including expression of liver-specific enzymes and the ability to support hepatitis C virus replication, making it a widely used model for liver cancer biology, drug metabolism, and infectious disease research. Huh-7 cells exhibit epithelial morphology and are suitable for studies of hepatocellular carcinoma progression, differentiation, and response to therapeutic agents.
DYNLT3 is a critical subunit of the cytoplasmic dynein motor complex, which drives microtubule-directed retrograde transport. Mechanistically, DYNLT3 integrates with dynein intermediate chain (DYNC1I) and heavy chain (DYNC1H) to form the motor core, and interacts with regulatory factors such as Lis1, NDE1, NDEL1, and BICD2 to coordinate cargo binding and motility. The gene is transcriptionally regulated by cell cycle transcription factors, including FOXM1 and E2F, and its product facilitates the intracellular trafficking of vesicles, organelles, and mitotic spindle assembly components. Disruption of DYNLT3 thus impairs dynein-mediated processes, affecting organelle positioning, vesicular transport, and mitotic progression.
In Huh-7 hepatocellular carcinoma cells, DYNLT3 loss-of-function provides insights into the role of dynein-dependent transport in liver cancer pathobiology. Given that aberrant mitotic spindle organization and defective intracellular trafficking are hallmarks of many cancers, this knockout model enables dissection of DYNLT3??s contribution to hepatocellular carcinoma proliferation, migration, and drug resistance. It is particularly relevant for investigating how dynein light chain dysfunction affects cell cycle regulation and the response to microtubule-targeting agents, which are under evaluation for liver cancer therapy.
This polyclonal knockout cell population is suitable for a range of assays, including Western blotting and RT-qPCR to confirm target disruption, immunofluorescence and live-cell imaging to visualize dynein-dependent transport and mitotic spindle defects, cell cycle analysis by flow cytometry, and drug sensitivity assays to evaluate responses to microtubule-directed chemotherapeutics. The model supports functional genomics studies of dynein in liver cancer, drug screening for modulators of intracellular trafficking, and mechanistic investigations into the interplay between cell division and transport pathways. For further details, please contact Ascent Research.
