DIP2A Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from the human SK-HEP-1 liver adenocarcinoma cell line, with disruption of the DIP2A gene. This population retains the heterogeneity of a non-clonal pool, offering a robust system for studying DIP2A deficiency without single-cell cloning bottlenecks. By avoiding clonal selection, the cells represent diverse editing outcomes, making them suitable for bulk functional studies including transcriptional regulation, signal transduction, and tumorigenesis.
The parental SK-HEP-1 cell line, originally isolated from ascitic fluid of a 52-year-old male with liver adenocarcinoma, is a hypertriploid epithelial model extensively used in cancer biology. SK-HEP-1 cells are a standard tool for studying hepatocellular carcinoma progression, metastasis, and angiogenesis, and their endothelial-like features facilitate tumor microenvironment research. Xenograft tumor formation and growth factor responsiveness make them ideal for investigating liver cancer aggressiveness.
DIP2A functions as a transcriptional coregulator that bridges transcription factors with chromatin-modifying complexes, directly interacting with DMAP1, DNMT1, and HDAC1. It operates downstream of ??-catenin/TCF and EGF signaling, transcriptionally regulating effectors such as MMP9, cyclin D1, c-Myc, Bcl-2, and PSD-95. By integrating Wnt/??-catenin and PI3K-AKT pathways, DIP2A modulates proliferation, survival, and matrix remodeling. The DIP2A-DMAP1 axis is critical for chromatin remodeling, and its disruption compromises these signaling cascades.
In the SK-HEP-1 context, DIP2A knockout provides a physiologically relevant model for tumor biology, given DIP2A??s implications in lung, gastric, and hepatocellular carcinomas. DIP2A overexpression correlates with enhanced proliferation, migration, and invasion; thus, its loss is expected to attenuate Wnt/??-catenin-driven cyclin D1 and c-Myc transcription, dampen AKT survival signaling, and reduce MMP9-dependent invasion. These polyclonal knockout cells enable interrogation of DIP2A??s roles in hepatocellular carcinogenesis, metastasis, and anoikis resistance, as well as chromatin regulator?Cdevelopmental signaling crosstalk.
Applications include mechanistic studies of tumor progression, drug screening, target validation, and Wnt/PI3K-AKT crosstalk analysis. The cells support assays such as Western blotting, RT-qPCR, RNA-seq, proliferation and invasion assays, co-immunoprecipitation, immunofluorescence, flow cytometry, and phospho-signaling analysis. They also serve as a model for neurodevelopmental disorder research, particularly in studying chromatin-remodeling gene networks. For additional technical details, ordering assistance, or customized solutions, please contact Ascent Research.
