The KIF2C Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited heterogeneous cell pool with disrupted KIF2C expression in the SK-HEP-1 hepatocellular carcinoma line. This polyclonal knockout population carries diverse gene disruptions introduced by CRISPR/Cas9, avoiding clonal artifacts while ensuring robust target-gene inactivation. The pool is suitable for functional assays without single-cell clone isolation, providing a physiologically relevant model for studying KIF2C loss-of-function.
SK-HEP-1 is a human liver adenocarcinoma cell line derived from the ascitic fluid of a patient, displaying adherent epithelial morphology and retaining key hepatocellular carcinoma features such as deregulated proliferation and metabolic adaptation. Widely used in hepatic cancer research, it provides a relevant platform for mechanistic studies and preclinical drug testing. Its established role in functional genomics makes it a reliable cellular context for knockout-based investigations.
KIF2C encodes MCAK, a microtubule-depolymerizing kinesin essential for faithful mitotic spindle assembly and chromosome segregation. MCAK activity is regulated through phosphorylation by upstream kinases Aurora B and PLK1, and it interacts with INCENP, Survivin, EB1, and CLASP1 to modulate microtubule dynamics and kinetochore attachments. Disruption of KIF2C leads to aberrant chromosome alignment, spindle checkpoint defects, and mitotic catastrophe. The KIF2C pathway involves core cell cycle regulators CDC20, CCNB1, and CDK1, and is transcriptionally activated by E2F1 and FOXM1.
In hepatocellular carcinoma, KIF2C knockout in SK-HEP-1 cells severely impairs mitotic progression, resulting in chromosome missegregation and markedly reduced proliferative capacity. This polyclonal model recapitulates the genetic heterogeneity of tumors, enabling robust studies on KIF2C-dependent signaling in cancer cell growth, migration, and survival. It also provides a platform to investigate synthetic lethal interactions with mitotic regulators overexpressed in liver cancer, such as PLK1 and Aurora B.
Researchers can apply this polyclonal knockout product in diverse assays, including Western blotting to confirm KIF2C depletion, immunofluorescence to visualize aberrant mitotic spindles, flow cytometry for cell cycle profiling, and colony formation or migration assays to assess tumorigenicity. Live-cell imaging enables real-time observation of microtubule dynamics and mitotic defects. This model is particularly suited for anti-mitotic drug screens, functional genomics, and evaluating KIF2C as a therapeutic target in hepatocellular carcinoma. For technical details or ordering, contact Ascent Research.
