DYNLT1 Knockout SK-HEP-1 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population derived from the SK-HEP-1 human hepatic adenocarcinoma line. This product provides a heterogeneous mixture of cells carrying targeted gene disruptions in DYNLT1, enabling loss-of-function analysis of the dynein light chain Tctex-type 1 subunit. The polyclonal format allows for rapid model generation without clonal selection, supporting pooled functional genomics and screening applications. CRISPR/Cas9-mediated gene disruption ensures stable knockout across the population while preserving the host cell’s genetic background.
The SK-HEP-1 cell line originates from the ascitic fluid of a patient with liver adenocarcinoma and is characterized by an endothelial-like phenotype, serving as a widely accepted model for liver sinusoidal endothelial cells. This line retains key hepatic features while expressing endothelial markers, offering a physiologically relevant system to study liver cancer biology, tumor-endothelial interactions, and hepatocellular carcinoma (HCC) progression.
DYNLT1 encodes a light chain subunit of the cytoplasmic dynein complex that functions as a cargo adaptor for retrograde microtubule-based transport. It directly interacts with dynein intermediate chain DYNC1I, light chain DYNLL1, and cargo adaptors BICD2 and NDEL1. Phosphorylation by CDK1 regulates mitotic spindle organization, while ZEB1 transcriptionally upregulates DYNLT1 in cancer. DYNLT1 mediates trafficking of TGF-?? receptor TGFBR2, the Wnt scaffold Dishevelled (DVL2), and transcription factor STAT3, thereby modulating TGF-??/SMAD and Wnt/planar cell polarity pathways. It is also essential for ciliogenesis, transporting proteins like RHODOPSIN to the ciliary axoneme.
In the SK-HEP-1 hepatic adenocarcinoma cell line, DYNLT1 knockout disrupts dynein-mediated trafficking of TGF-?? receptors and Dishevelled, offering a valuable model to investigate liver cancer progression and endothelial-like phenotypes. Loss of DYNLT1 alters TGF-??/SMAD and Wnt/planar cell polarity signaling, impacting epithelial-mesenchymal transition (EMT), cell migration, and ciliary assembly. This polyclonal knockout population reflects the heterogeneity of tumor cells, facilitating studies of HCC invasion, metastatic potential, and drug sensitivity within a mixed genetic background.
This knockout model is applicable to a range of studies, including dynein-mediated transport in liver cancer, TGF-?? and Wnt signaling crosstalk, ciliogenesis, and drug sensitivity assays. Compatible techniques include immunoblotting for DYNLT1 and dynein subunits, immunofluorescence for ciliary acetylated tubulin, flow cytometry for cell cycle profiling, transwell migration assays, and co-immunoprecipitation of dynein complex components. Phospho-SMAD2 ELISA can assess TGF-?? pathway activity, and RT-qPCR provides rapid knockout validation. For further details, contact Ascent Research.
