The GPS2 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from the human liver adenocarcinoma cell line SK-HEP-1, engineered for disruption of the GPS2 gene. This polyclonal knockout pool contains a heterogeneous mixture of cells carrying various loss-of-function mutations, providing a robust model to study GPS2’s role without clonal bias. Suitable for experiments that benefit from population-level genetic diversity and functional gene ablation in a hepatic carcinoma context.
SK-HEP-1 cells were isolated from the ascites of a patient with liver adenocarcinoma and are widely used as a hepatocellular carcinoma model. They exhibit epithelial morphology, rapid proliferation, and aberrant activation of growth and survival pathways characteristic of liver cancer. This background makes them ideal for investigating tumor suppressor genes and oncogenic signaling in hepatocellular carcinoma.
GPS2 functions as a transcriptional corepressor that suppresses JAK-STAT, NF-??B, and MAPK signaling by recruiting HDAC3-containing corepressor complexes to target promoters. It interacts with NCOR1, TBL1X, and TBL1XR1, and is regulated by upstream signals TNF, IL6, and PPARG. GPS2 directly interacts with transcription factors STAT3 and NFKB1, and represses downstream effectors including IL6, TNF, MMP9, CDKN1A, and BCL2L1. Knockout of GPS2 is expected to relieve repression, leading to hyperphosphorylation of STAT3, increased NF-??B activity, and upregulation of genes promoting proliferation, survival, and inflammation.
In SK-HEP-1 cells, loss of GPS2-mediated repression further amplifies oncogenic signaling, driving cell cycle progression and resistance to apoptosis. This model is valuable for dissecting the tumor-suppressive function of GPS2 in hepatocellular carcinoma and for exploring its cross-talk with DNA damage response pathways. The polyclonal composition ensures that observed phenotypes are representative and not artifacts of clonal selection.
Applications include mechanistic studies of GPS2-regulated pathways, drug screening for liver cancer therapies, and functional assays such as western blot for phospho-STAT3, NF-??B luciferase reporter assays, cell viability and apoptosis flow cytometry, RT-qPCR of target genes, and migration assays. Researchers can utilize this model to test inhibitors of JAK/STAT or NF-??B or to perform genetic screens. For further inquiries, contact Ascent Research.
