The KIF1B Knockout SK-HEP-1 Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human hepatocellular carcinoma line SK-HEP-1, engineered for disruption of the KIF1B gene. This heterogeneous knockout model enables functional loss-of-function studies of the kinesin motor protein KIF1B, which is implicated in organelle transport and tumor suppression. The polyclonal nature captures a spectrum of editing events, facilitating robust population-level analyses of gene function in a widely used liver cancer background.
SK-HEP-1 is a well-characterized human hepatocellular carcinoma cell line originally isolated from the ascitic fluid of a patient with adenocarcinoma of the liver. These adherent cells exhibit an aneuploid karyotype and are highly tumorigenic in vivo, making them a standard model for hepatocellular carcinoma (HCC) research. Their robust growth characteristics and well-documented molecular profile render SK-HEP-1 an ideal system for dissecting oncogenic mechanisms and evaluating potential therapeutic vulnerabilities in liver cancer.
KIF1B encodes a microtubule-dependent kinesin motor protein with two major isoforms: KIF1B??, which mediates anterograde transport of mitochondria, and the tumor suppressor KIF1B??, which promotes apoptosis through formation of a ternary complex with the calcium-binding protein CHP1 and the vesicle fusion factor NSF. Upon activation by upstream Ca2+ signals, KIF1B?? recruits CHP1 and NSF to mitochondria, triggering caspase-3 activation and apoptotic cell death. Consequently, KIF1B?? functions as a critical negative regulator of cell survival, and its loss is associated with neuroblastoma and other malignancies.
Disruption of KIF1B in the SK-HEP-1 hepatocellular carcinoma background is predicted to impair apoptotic signaling and alter mitochondrial distribution, thus conferring a survival advantage that mirrors oncogenic transformation. This knockout model enables dissection of KIF1B??-mediated tumor suppression specifically within liver cancer, where dysregulation of mitochondrial homeostasis and apoptosis evasion are hallmark features. By comparing wild-type and knockout populations, researchers can interrogate how loss of KIF1B function influences SK-HEP-1 proliferation, migration, and drug sensitivity.
Typical experimental applications include assessing apoptosis susceptibility via Annexin V staining and caspase-3 activation assays, evaluating mitochondrial integrity using mitochondrial membrane potential dyes and immunofluorescence for organelle markers, and profiling cell growth inhibition through proliferation assays. Additionally, Transwell migration and invasion assays can elucidate the impact of KIF1B loss on metastatic potential, while RT-qPCR and Western blotting confirm downstream signaling changes. This polyclonal knockout population serves as a valuable tool for drug sensitivity screening and for further CRISPR gene editing studies aimed at dissecting mitochondrial-encoded signaling pathways. For further information or to place an order, please contact Ascent Research.
