The HTATIP2 Knockout SK-HEP-1 Polyclonal Cells represent a heterogeneous CRISPR/Cas9-edited population in which the HTATIP2 gene locus has been disrupted, creating a functional knockout model in the SK-HEP-1 human liver adenocarcinoma background. This polyclonal format provides a practical loss-of-function system without single-cell clonal isolation, enabling researchers to investigate TIP30 tumor suppressor biology in a physiologically relevant hepatocarcinoma context. The product is supplied as a ready-to-use polyclonal knockout cell pool, optimized for robust gene disruption and suitable for a wide range of downstream molecular and cellular assays.
SK-HEP-1 is an immortalized cell line originally derived from ascitic fluid of a patient with liver adenocarcinoma. This line exhibits a unique blend of epithelial and endothelial characteristics, making it a favored model for studying hepatocellular carcinoma (HCC) biology, tumor angiogenesis, and metastatic dissemination. SK-HEP-1 cells display aggressive growth, invasiveness, and angiogenic potential, traits that are further accentuated upon HTATIP2 ablation. The cell line??s adaptability to standard culture conditions and its extensive use in cancer research ensure reliable experimental reproducibility and accessible validation across laboratories.
HTATIP2, encoding the TIP30 protein, acts as a multifaceted tumor suppressor and transcriptional cofactor. Mechanistically, TIP30 is activated by TP53 and functions downstream of E2F1, integrating signals from hypoxia and DNA damage. It directly interacts with RNA polymerase II subunit RPB5 and the HIV-1 Tat protein, modulating transcriptional initiation and elongation. In the apoptotic cascade, TIP30 promotes BAX expression while repressing BCL2, leading to Caspase-3 activation and programmed cell death. Additionally, TIP30 suppresses angiogenesis by transcriptionally downregulating VEGF and attenuating MMP9 expression, thereby inhibiting endothelial tube formation and invasive behavior.
In the SK-HEP-1 background, HTATIP2 knockout exacerbates the cell line??s intrinsic tumorigenic properties. Loss of TIP30 disrupts the p53/TIP30/Bax apoptotic axis, conferring resistance to cell death and promoting unchecked proliferation. Concurrently, derepression of VEGF and MMP9 enhances angiogenic signaling and invasive capacity, mirroring aggressive HCC phenotypes. This polyclonal knockout model therefore recapitulates key hallmarks of liver cancer progression, including evasion of apoptosis, sustained angiogenesis, and enhanced metastatic potential, providing a biologically relevant platform for mechanistic and translational studies.
This HTATIP2 knockout product is ideally suited for investigating hepatocellular carcinoma pathobiology, tumor suppressor gene networks, and cancer drug resistance. Typical applications include proliferation assays (CCK-8), invasion studies (Boyden chamber), apoptosis quantification (flow cytometry), and endothelial tube formation assays. The model also supports transcriptional analyses via ChIP-qPCR and protein?Cprotein interaction studies such as co-immunoprecipitation. Additionally, it enables screening of therapeutic compounds targeting p53, VEGF, or associated pathways. For detailed protocols, customized assay design, or ordering information, please contact Ascent Research.
