The KIF3B Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human SK-HEP-1 hepatic adenocarcinoma cell line. This product provides a loss-of-function model for the KIF3B gene, which encodes a motor protein of the kinesin-2 complex. The polyclonal nature ensures a heterogeneous pool of edited cells, suitable for robust population-level studies without the biases of clonal selection. This model enables investigation of KIF3B-dependent processes in a human liver cancer context.
SK-HEP-1 is a well-characterized human hepatic adenocarcinoma cell line originally isolated from the ascitic fluid of a patient with hepatocellular carcinoma. These adherent, epithelial-derived cells maintain malignant properties and are widely used as a model for liver cancer cell biology. Their origin from ascites??a common complication of advanced HCC??makes them particularly relevant for studying metastatic behavior and signaling mechanisms that drive tumor progression in the hepatic microenvironment.
KIF3B functions as the motor subunit of the heterotrimeric kinesin-2 complex, together with KIF3A and the adaptor KAP3 (KIFAP3). This motor drives anterograde intraflagellar transport (IFT) along axonemal microtubules, a process essential for the assembly and maintenance of primary cilia. Transcription of KIF3B is regulated by ciliogenic factors such as FOXJ1, RFX2, and RFX3. Within the cilium, KIF3B-containing kinesin-2 interacts with IFT particles (e.g., IFT88, IFT140) and BBS proteins to transport cargo, including signaling components of the Hedgehog and Wnt pathways. In the Hedgehog pathway, kinesin-2-mediated transport is required for the proper localization and activation of SMO and the downstream GLI transcription factors, with SUFU acting as a negative regulator. Similarly, KIF3B influences the Wnt pathway by facilitating the trafficking of beta-catenin-containing vesicles, thereby modulating the transcriptional activity of beta-catenin. Thus, KIF3B links microtubule-based motor activity to the output of key developmental signaling networks.
In SK-HEP-1 cells, KIF3B knockout disrupts ciliary biogenesis and impairs signaling through the Hedgehog and Wnt pathways, both of which are frequently hyperactivated in hepatocellular carcinoma. This polyclonal knockout model allows researchers to dissect the specific contributions of KIF3B to cancer cell behaviors such as migration, invasion, and proliferation, all of which are influenced by ciliary and vesicle trafficking. By comparing the polyclonal knockout population to parental or control cells, investigators can evaluate the dependence of these processes on KIF3B motor function and identify compensatory or parallel mechanisms that sustain malignant phenotypes.
This product is suitable for a wide range of experimental techniques. Western blotting and RT-qPCR can be used to confirm KIF3B disruption, while immunofluorescence staining for ciliary markers (e.g., acetylated ??-tubulin, IFT88) allows assessment of ciliogenesis. Functional studies can employ transwell migration assays to measure cell motility, cell proliferation assays (such as MTT or EdU incorporation), and Gli-luciferase reporter assays to quantify Hedgehog pathway activity. Flow cytometry enables cell cycle and apoptosis analysis, and the polyclonal format is amenable to high-throughput screening for ciliogenesis modulators or signaling inhibitors. For further information or to discuss your specific experimental requirements, please contact Ascent Research.
