The GTSE1 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the SK-HEP-1 hepatic adenocarcinoma cell line. This model harbors a targeted disruption of the GTSE1 gene, resulting in loss of GTSE1 protein function. The polyclonal format provides a mixed population of edited cells, enabling the study of GTSE1 deficiency in a heterogeneous context without clonal selection bias. This system allows direct investigation of GTSE1’s role in cell cycle progression and p53-mediated stress responses across diverse genetic backgrounds.
The parental SK-HEP-1 line, originally established from ascitic fluid of a liver adenocarcinoma patient, is a widely used model for hepatocellular carcinoma (HCC). These adherent cells exhibit dysregulated proliferation, metastatic potential, and altered apoptotic signaling, making them well-suited for studying HCC pathobiology and drug resistance mechanisms. The introduction of GTSE1 knockout in this background creates a powerful platform to dissect the contribution of this gene to liver cancer aggressiveness and therapeutic response.
GTSE1 regulates G2/M progression by inhibiting p53 transcriptional activity and promoting its degradation, while also binding EB1 and microtubules to control mitotic spindle dynamics. Loss of GTSE1 stabilizes p53, inducing p21, BAX, and PUMA expression, leading to cell cycle arrest and apoptosis. This integrates DNA damage and E2F1 signals to modulate Cyclin B1/CDK1 activity.
In the context of hepatic adenocarcinoma, GTSE1 overexpression correlates with tumor aggressiveness and chemoresistance. The SK-HEP-1 GTSE1 knockout cells thus provide a relevant model to study sensitization to DNA-damaging agents and restoration of p53-dependent tumor suppression. Researchers can evaluate reactivation of p53 signaling, including p21-mediated growth inhibition and BAX/PUMA-driven apoptosis, as well as investigate mitotic defects such as aberrant spindle morphology and chromosome missegregation arising from disrupted microtubule dynamics.
These cells support Western blotting for p53, p21, BAX, and PUMA; immunofluorescence for microtubule and EB1 localization; flow cytometry for cell cycle distribution and apoptosis (annexin V); and drug sensitivity testing with chemotherapeutics like doxorubicin and cisplatin. These applications enable mechanistic studies of GTSE1 in cell cycle control, p53 signaling, and chemoresistance. For technical inquiries or custom requests, please contact Ascent Research.
