The KIF13B Knockout SK-HEP-1 Polyclonal Cells product provides a polyclonal population of SK-HEP-1 human liver adenocarcinoma cells bearing CRISPR/Cas9-mediated KIF13B gene disruption. This knockout model preserves the parental cell line??s background while introducing genetic heterogeneity reflective of a mixed edited population, enabling researchers to study KIF13B loss-of-function effects without the limitations of a single clone. The gene editing strategy targets the KIF13B locus to ablate normal kinesin motor protein expression.
Originally derived from the ascites of a patient with liver adenocarcinoma, the SK-HEP-1 cell line is a versatile model for hepatocellular carcinoma pathobiology and metastatic dissemination. These cells carry relevant oncogenic mutations and demonstrate high motility and invasiveness in vitro and in vivo, recapitulating key aspects of tumor progression. The SK-HEP-1 system is thus an ideal host for studying the contribution of the KIF13B kinesin to intracellular trafficking processes that underpin liver cancer cell migration and invasion.
KIF13B encodes a plus-end-directed kinesin-3 motor that transports Rab11-positive recycling endosomes along microtubules, delivering adhesion molecules including integrin ??1 (ITGB1) and VE-cadherin (CDH5) to the plasma membrane. This process regulates focal adhesion turnover, cell migration, and angiogenesis. KIF13B interacts with RAB11A, RAB11B, the AP-1 adaptor complex, and MYO5A. Upstream, VEGFR2 and SRC kinase activate this trafficking pathway; downstream, ITGB1 and CDH5 surface presentation control cell adhesion and motility. KIF13B thus integrates signals from endocytic recycling and VEGF pathways to drive migration.
Disruption of KIF13B function in the SK-HEP-1 hepatocellular carcinoma model is anticipated to impair recycling endosome distribution and delay the delivery of adhesion receptors to the plasma membrane, leading to diminished cell motility and reduced invasive potential. This knockout cell population therefore offers a powerful tool to dissect how kinesin motor proteins contribute to liver cancer malignancy and to evaluate the therapeutic potential of targeting the KIF13B-Rab11 trafficking axis. The model is particularly suited for studying the interplay between endosomal transport and focal adhesion dynamics in a metastatic context.
Key applications include investigating the role of KIF13B-dependent vesicular transport in liver cancer cell migration, validating the motor protein as a drug target for anti-metastatic therapy, and screening small molecules that interfere with kinesin?Ccargo binding. Recommended assays include Western blot and RT-qPCR for knockout verification, immunofluorescence for endosome and microtubule organization, Boyden chamber and wound-healing migration/invasion assays, flow cytometry for surface ITGB1, and co-immunoprecipitation with RAB11 isoforms. The polyclonal knockout format enables studies of population-level effects. For technical and custom service inquiries, contact Ascent Research.
