The ASCC2 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited human hepatic adenocarcinoma cell population in which the ASCC2 gene has been disrupted. This polyclonal knockout pool is generated by Cas9-mediated genome editing, introducing heterogeneous loss-of-function mutations in ASCC2 across the cell population. The product provides a robust model for studying ASCC2-dependent processes without isolating single-cell clones, thereby capturing the diversity of functional ablation within a cancer cell context.
The host cell line, SK-HEP-1, is an ascites-derived liver adenocarcinoma cell line widely used as a model for hepatic cancer and drug metabolism. This cell line exhibits characteristics of hepatocellular carcinoma, enabling investigation of liver tumor biology and xenobiotic processing. Its continuous proliferation and well-characterized genomic landscape make it suitable for genetic perturbation studies, particularly in the context of DNA repair and cancer cell survival mechanisms.
ASCC2 (Activating Signal Cointegrator 1 Complex Subunit 2) is an integral component of the ASC?1 (Activating Signal Cointegrator 1) complex, which also includes ASCC1 and ASCC3. This complex is critical for DNA alkylation damage repair, where it is recruited by the DNA repair enzyme ALKBH3 to sites of alkylated DNA lesions. Once localized, the ASC?1 complex facilitates dealkylation repair through base excision repair machinery, thereby maintaining genomic integrity under alkylation stress. Beyond repair, ASCC2 participates in transcriptional coactivation, notably influencing NF?kappaB signaling, linking DNA damage responses to transcriptional regulation. Upstream regulators include DNA alkylating agents and DNA damage signaling cascades, while downstream effects involve cell survival and repair of alkylated DNA bases. Direct interacting partners include ASCC1, ASCC3, and ALKBH3, underscoring its central role in the alkylation damage response.
In the SK-HEP-1 hepatic cancer model, disruption of ASCC2 is particularly relevant for hepatocellular carcinoma research, where alkylation damage sensitivity and chemoresistance are key clinical challenges. The polyclonal knockout cells allow examination of how loss of ASCC2 function impacts tumor cell viability, apoptosis, and DNA repair proficiency under chemotherapeutic stress, such as treatment with alkylating agents. This model is invaluable for dissecting the interplay between the DNA damage response and oncogenic signaling pathways in liver cancer.
This product is suitable for a range of experimental applications, including DNA damage response studies, chemosensitivity profiling, and alkylation repair pathway analysis. Researchers can employ quantitative assays such as RT-qPCR and western blotting to assess gene and protein expression changes, comet assays and immunofluorescence for DNA damage detection, and colony formation or cell viability assays under alkylation stress. Apoptosis assays further enable interrogation of cell death pathways. For additional technical information, please contact Ascent Research.
