This CRISPR/Cas9-edited polyclonal cell population provides a loss-of-function model for KIF1C, a plus-end-directed microtubule motor protein, in the SK-HEP-1 hepatic adenocarcinoma cell line. The polyclonal format comprises a heterogeneous mix of gene-disrupted cells, enabling robust functional studies without the constraints of clonal selection. By disrupting KIF1C, the model permits investigation of its roles in organelle transport, cell adhesion, and migration. This product is intended for advanced research into the molecular mechanisms of intracellular trafficking and cancer cell motility.
The host cell line, SK-HEP-1, is a well-characterized human hepatic adenocarcinoma line originally isolated from ascitic fluid of a patient with liver adenocarcinoma. These cells exhibit a unique phenotype with both endothelial and mesenchymal features, making them a valuable model for studying tumor cell plasticity, epithelial-to-mesenchymal transition, and metastasis. SK-HEP-1 cells are widely used in cancer research due to their robust proliferative and invasive properties, providing a relevant background for investigating the functional significance of motor proteins like KIF1C in liver cancer progression.
Molecularly, KIF1C is a kinesin-3 motor that transports vesicles and organelles along microtubules, regulating integrin recycling and focal adhesion turnover. Its activity is controlled by Rho GTPases and kinases, and it operates downstream of microtubule dynamics. KIF1C interacts with microtubules, RAB1A, 14-3-3 proteins, and kinesin light chains for cargo transport, while also binding integrins and focal adhesion kinase to modulate migration. Disruption of KIF1C impairs vesicular trafficking, focal adhesion dynamics, and cell motility.
In the SK-HEP-1 adenocarcinoma background, KIF1C knockout is highly relevant for studying liver cancer metastasis. The mesenchymal and invasive traits of this line make it suitable for examining how KIF1C loss attenuates migration and invasion by disrupting focal adhesion turnover and integrin recycling. The model also enables investigation of KIF1C’s role in drug resistance and provides insights into hereditary spastic paraplegia, where KIF1C mutations are causative.
These polyclonal KIF1C knockout cells are well-suited for functional studies using wound healing and transwell migration assays to assess motility, immunofluorescence to examine focal adhesion dynamics, western blotting for integrin expression, and vesicle tracking for transport processes. They provide a robust model for research on microtubule-based trafficking, cancer cell migration, and the mechanisms of KIF1C-linked disorders. For inquiries, please contact Ascent Research.
