The HECA Knockout SK-HEP-1 Polyclonal Cells provide a versatile CRISPR/Cas9-mediated gene disruption model targeting the HECA gene in the human SK-HEP-1 cell line. This polyclonal knockout cell population contains a heterogeneous collection of edited alleles, eliminating the biases associated with single-cell cloning and enabling robust functional analysis. The product is intended for investigating the role of the cell cycle regulator HECA in liver cancer biology, particularly in the context of hepatocellular carcinoma.
The SK-HEP-1 host cell line was derived from the ascites of a patient with hepatic adenocarcinoma and is widely employed as a hepatocellular carcinoma model despite its endothelial-like characteristics. These adherent epithelial cells exhibit rapid proliferation and have been extensively used to study oncogenic signaling and drug responses in liver cancer. Their tumorigenic origin and well-characterized growth properties make SK-HEP-1 an ideal platform for examining the functional consequences of HECA ablation on cell cycle progression and tumor cell behavior.
HECA encodes a protein that acts as a critical modulator of the G1/S cell cycle transition by interacting directly with cyclin-dependent kinases CDK2 and CDK3. Within the signaling network, HECA is regulated by upstream transcription factors such as E2F and p53, as well as cyclins CCNE1 and CCNA2. Its disruption has been shown to alter the kinase activity of CDK2 and CDK3, leading to aberrant phosphorylation of RB1 and dysregulation of E2F target genes, including CCNE1 and CCNA2. The protein also interfaces with CDK inhibitors like p21, thereby integrating signals from the p53-p21 checkpoint and the RB-E2F axis to tightly control cell cycle entry.
Knockout of HECA in SK-HEP-1 cells is expected to perturb the CDK2-CCNE1 complex and the RB-E2F regulatory loop, providing a model system to dissect the mechanisms underlying uncontrolled proliferation in hepatocellular carcinoma. Because this liver cancer cell line frequently harbors alterations in p53 and RB pathways, the HECA knockout offers a physiologically relevant background to study how loss of this cell cycle regulator cooperates with existing oncogenic lesions. Researchers can use this model to explore the dependency of liver tumor cells on HECA for proliferation and survival, potentially uncovering novel therapeutic vulnerabilities.
This polyclonal knockout cell product supports a wide range of experimental applications in academic and pharmaceutical research. Investigators can employ Western blotting to monitor changes in cell cycle markers, flow cytometry to assess DNA content distribution, and RT-qPCR to quantify expression of E2F target genes. Co-immunoprecipitation assays can be used to validate disrupted HECA-CDK2 or HECA-CDK3 interactions, while proliferation assays such as MTT or BrdU incorporation measure growth phenotypes. Additional applications include ChIP-qPCR to examine E2F binding at target gene promoters and drug screening campaigns to identify compounds that selectively affect HECA-deficient liver cancer cells. For further technical details or ordering information, please contact Ascent Research.
