The CCDC127 Knockout SK-HEP-1 Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population in which the CCDC127 gene has been disrupted. This loss-of-function model is generated in the SK-HEP-1 human hepatic adenocarcinoma cell line and is supplied as a mixed population of edited cells, suitable for functional studies requiring heterogeneous gene knockout backgrounds. The disruption of CCDC127 eliminates its tumor-suppressive functions, allowing investigation of oncogenic signaling pathways.
The SK-HEP-1 cell line is an adherent epithelial line derived from the ascites fluid of a male patient with liver adenocarcinoma. Widely employed as a hepatocellular carcinoma (HCC) model, these cells exhibit characteristics of advanced liver cancer and are extensively used in studies of tumor biology, metastasis, and drug resistance. Their robust growth and well-characterized signaling networks make them an ideal platform for dissecting the molecular mechanisms of HCC progression.
CCDC127 functions as a tumor suppressor in hepatocellular carcinoma by negatively regulating Wnt/??-catenin and PI3K/AKT signaling. It interacts with ??-catenin, GSK3??, and Axin, preventing ??-catenin nuclear translocation and reducing TCF/LEF-mediated transcription. Consequently, the expression of oncogenic targets such as Cyclin D1, c-Myc, MMP2, and MMP9 is suppressed. Additionally, CCDC127 activity influences epithelial-mesenchymal transition (EMT) markers including E-cadherin, N-cadherin, and Vimentin. The gene is frequently silenced in HCC through promoter methylation and histone deacetylation, leading to unchecked activation of these downstream pathways.
In the SK-HEP-1 background, disruption of CCDC127 mimics the epigenetic silencing observed in clinical HCC specimens, thereby recreating a tumor-permissive cellular environment. This polyclonal knockout model recapitulates the loss of CCDC127-mediated growth suppression, leading to enhanced cell proliferation, migration, and invasiveness. The concomitant upregulation of Wnt/??-catenin and PI3K/AKT/mTOR signaling makes these cells valuable for investigating the molecular drivers of HCC aggressiveness and for testing therapeutic interventions targeting these pathways.
This polyclonal knockout product is well-suited for a wide range of functional analyses, including Western blotting and RT-qPCR to confirm downstream target modulation, CCK-8 and wound healing assays for proliferation and migration phenotyping, transwell invasion assays, and TOP/FOP flash reporter assays to quantify ??-catenin/TCF transcriptional activity. It also supports ChIP-qPCR for ??-catenin target occupancy, immunofluorescence localization of EMT markers, and transcriptome-wide RNA-seq profiling. Additionally, the model enables drug sensitivity screening with agents such as sorafenib to identify synergy between Wnt inhibition and standard HCC therapies. For further technical details, please contact Ascent Research.
