The CCDC6 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from the human liver adenocarcinoma cell line SK-HEP-1. This gene-disrupted model enables robust loss-of-function analyses of CCDC6 without requiring clonal isolation. The polyclonal format provides a diverse knockout pool suitable for functional studies in a tumorigenic background.
SK-HEP-1 is an established cell line originating from a liver adenocarcinoma, historically classified as hepatocellular carcinoma. These adherent epithelial cells are tumorigenic and widely used for investigating hepatic cancer biology, drug metabolism, and oncogenic signaling. The hepatocellular origin makes this background particularly relevant for dissecting tumor suppressor pathways and apoptotic mechanisms in liver cancer.
CCDC6 is a tumor suppressor that integrates DNA damage signaling and apoptosis. Activated by ATM/ATR kinases in response to DNA double-strand breaks, CCDC6 functions downstream to promote p53/BAX-mediated apoptosis and inhibit BCL2. It also acts as a CREB1 transcriptional coactivator, modulating expression of survival genes. Interaction with 14-3-3 proteins regulates CCDC6 subcellular localization. In thyroid cancer, the RET/PTC1 fusion replaces the tumor-suppressive domain with oncogenic RET kinase.
In the SK-HEP-1 liver adenocarcinoma context, CCDC6 knockout permits investigation of tumor suppressor loss in a hepatic environment. This model is valuable for studying resistance to DNA-damaging chemotherapeutics and for elucidating how impaired apoptosis contributes to hepatocellular carcinoma progression. Additionally, the interplay between CCDC6 and CREB1 signaling can be explored to identify novel therapeutic targets specific to liver malignancies.
Researchers can employ this polyclonal knockout product for Western blotting and RT-qPCR to analyze protein and transcript changes, immunofluorescence to examine CCDC6 localization, and apoptosis assays using Annexin V. DNA damage response can be assessed via ??H2AX foci formation, while CREB reporter assays elucidate transcriptional effects. Clonogenic survival assays are suitable for testing drug sensitivity. Applications include studies of tumor suppression, DNA repair, and liver cancer biology. For further inquiries, contact Ascent Research.
