The JTB Knockout SK-HEP-1 Polyclonal Cells from Ascent Research represent a CRISPR/Cas9-edited polyclonal knockout cell population in which the JTB gene has been disrupted in the SK-HEP-1 human liver adenocarcinoma cell line. This polyclonal knockout model is generated using CRISPR/Cas9-mediated gene disruption, generating a heterogeneous loss-of-function population without clonal selection, thereby preserving biological variability and avoiding clone-specific artifacts. The product is supplied as a ready-to-use polyclonal pool of knockout cells, optimized for immediate application in functional genomics, cancer biology, and signal transduction studies.
SK-HEP-1 cells are an established epithelial cell line derived from the ascitic fluid of a patient with liver adenocarcinoma and serve as a widely employed model for hepatocellular carcinoma (HCC). These cells retain key molecular features of liver cancer, including aberrant proliferation, migratory capacity, and altered apoptotic signaling, making them highly relevant for dissecting oncogenic mechanisms. The SK-HEP-1 background provides a clinically pertinent context to investigate JTB function in HCC, where dysregulation of cytokinesis and mitochondrial apoptosis pathways frequently contributes to tumor progression and drug resistance.
JTB (Jumping Translocation Breakpoint) encodes a protein that localizes to the mitotic spindle and midbody, where it plays a critical role in cytokinesis. Mechanistically, JTB function is regulated by CDK1 and Aurora B kinase, and it interacts with ??-tubulin and the Hippo pathway scaffold SAV1 (Salvador homolog 1). JTB modulates cytokinesis completion and acts upstream of Caspase-3 activation and cytochrome c release upon mitochondrial translocation. Within the Hippo signaling network, JTB influences the kinase cascade involving MST1 and LATS1, which converge on the transcriptional coactivator YAP. Overexpression of JTB’s cytoplasmic domain promotes apoptosis, linking JTB to both mitotic regulation and programmed cell death. These molecular interactions position JTB at the intersection of cell cycle progression, Hippo signaling, and apoptosis, making it a node for therapeutic targeting in malignancies.
In the SK-HEP-1 hepatocellular carcinoma context, disruption of JTB provides a powerful tool to examine how loss of cytokinesis control and Hippo pathway modulation impact liver cancer cell behavior. Because SK-HEP-1 cells exhibit active proliferation and metastatic potential, the JTB knockout model enables dissection of aberrant midbody assembly, mitotic fidelity, and YAP-dependent transcription. Given that Hippo pathway dysregulation is a hallmark of HCC, and mitochondrial dysfunction underlies chemoresistance, this model allows direct investigation of JTB’s role in coupling cell division to apoptotic sensitivity. Researchers can assess how JTB loss alters colony formation, anoikis resistance, and response to mitotic inhibitors, thereby advancing the mechanistic understanding of HCC pathogenesis.
This polyclonal knockout cell population is ideally suited for a broad range of experimental applications. Cytokinesis analysis can be performed via immunofluorescence microscopy of midbody markers or live-cell imaging of mitotic progression. Apoptosis studies employing Annexin V flow cytometry or Caspase-3 activation assays directly probe JTB’s pro-apoptotic functions. The model enables Hippo pathway investigation through YAP localization assays and co-immunoprecipitation of JTB-SAV1 complexes. Additionally, wound healing migration assays and Western blotting of cell cycle regulators (Cyclin B, CDK1, Aurora B) facilitate drug screening studies targeting mitotic kinases. The heterogeneous knockout population is particularly valuable for evaluating polyclonal responses to therapeutics in HCC research. For further details on assay optimization or custom applications, please contact Ascent Research.
