The KLC4 Knockout SK-HEP-1 Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of the KLC4 gene in the SK-HEP-1 human hepatic adenocarcinoma cell line. This heterogeneous pool of gene-disrupted cells constitutes a loss-of-function model for kinesin light chain 4 (KLC4). Gene disruption was achieved via CRISPR/Cas9, and protein ablation can be verified by Western blot or immunofluorescence, ensuring reliable use in downstream functional assays.
SK-HEP-1 is an established cell line derived from the ascitic fluid of a patient with liver adenocarcinoma. Despite its hepatic origin, it displays endothelial-like characteristics such as tube formation and endothelial marker expression, making it a unique model for studying tumor cell plasticity, adhesion, and metastasis. This line is widely employed in hepatocellular carcinoma research, offering a relevant background for investigating molecular mechanisms that drive liver cancer invasion and dissemination.
KLC4 encodes a light chain subunit of the kinesin-1 motor complex, which partners with heavy chains KIF5A and KIF5B to facilitate anterograde microtubule-based transport of vesicles, mitochondria, and signaling cargoes. KLC4 directly binds the adaptor protein JIP3, which scaffolds JNK pathway components. Loss of KLC4 disrupts kinesin-1 function, leading to mislocalization of JIP3 and subsequent dysregulation of JNK signaling. This alters phosphorylation of downstream targets and transcriptional programs that govern cell migration, proliferation, and apoptosis, providing a tool to dissect transport-dependent signal regulation.
In SK-HEP-1 cells, which combine hepatic and endothelial features, KLC4 knockout illuminates the role of intracellular transport in motility, invasion, and metastatic potential. Impaired kinesin-1 activity disrupts organelle distribution and may alter mitochondrial positioning, affecting metabolic adaptation within the tumor microenvironment. This model is therefore particularly suited for examining how transport defects contribute to transendothelial migration and liver cancer dissemination.
This polyclonal knockout cell population supports diverse applications: live-cell imaging of mitochondrial motility, immunofluorescence-based organelle tracking, JNK phosphorylation analysis via Western blot or ELISA, and wound healing migration assays. It also enables drug sensitivity screening to identify compounds targeting kinesin-dependent processes or JNK signaling. Researchers in liver cancer metastasis, intracellular trafficking, and signal transduction will find this resource valuable. For technical inquiries, please contact Ascent Research.
