The ING5 Knockout SK-HEP-1 Polyclonal Cells constitute a CRISPR/Cas9-mediated gene disruption model designed to ablate ING5 expression in the SK-HEP-1 human hepatocellular carcinoma cell line. This product is supplied as a polyclonal knockout cell population, representing a heterogeneous pool of edited cells generated through non-homologous end joining repair pathways following Cas9 nuclease activity at the ING5 genomic locus. The mixed genotype composition avoids clonal bias while retaining sufficient target gene inactivation for loss-of-function studies at the population level. Researchers can employ this model to dissect ING5-dependent tumor suppressive mechanisms in a liver cancer context. The system is compatible with standard mammalian cell culture workflows and downstream functional assays.
SK-HEP-1 is a well-characterized cell line originally derived from the ascites fluid of a patient with liver adenocarcinoma. As an aneuploid male cell line with epithelial morphology, it serves as a validated in vitro platform for hepatocellular carcinoma research, exhibiting hallmark features such as anchorage-independent growth and tumorigenicity in xenograft models. Its hepatic origin makes it particularly relevant for investigating molecular pathways deregulated in liver cancers, including p53 signaling, chromatin remodeling, and apoptotic responses. The SK-HEP-1 background provides a pathophysiologically appropriate host for examining how ING5 loss contributes to hepatocarcinogenesis and treatment resistance.
ING5 functions as a type II tumor suppressor through its role as a core subunit of the HBO1 (KAT7) histone acetyltransferase complex, which catalyzes histone H3 and H4 acetylation to open chromatin structure and facilitate transcriptional activation. ING5 directly interacts with p53 and enhances p53-dependent transcription of key downstream targets such as the cyclin-dependent kinase inhibitor p21/CDKN1A and the pro-apoptotic effector BAX. This cooperation leads to cell cycle arrest at G1/S and induction of programmed cell death. Upstream, ING5 expression is regulated by p53 itself and by E2F transcription factors, establishing a feed-forward loop that reinforces tumor suppression. ING5 also associates with other HBO1 complex components including JADE and BRPF scaffold proteins, and functionally cooperates with Tip60 in DNA damage response pathways. Disruption of ING5 impairs histone acetylation dynamics, attenuates p53-mediated transcription, and compromises repair of double-strand breaks, collectively compromising genome stability.
In the SK-HEP-1 hepatocellular carcinoma model, ING5 knockout allows dissection of how loss of this tumor suppressor alters epigenetic landscapes and transcriptional programs relevant to liver cancer progression. The polyclonal knockout population can reveal dominant-negative effects, dosage sensitivities, or compensatory mechanisms that may be masked in monoclonal isolates. Because SK-HEP-1 cells harbor wild-type p53, they are particularly suited to evaluate ING5-mediated transactivation of p53 targets such as p21 and BAX. This model enables investigation of the interplay between ING5 and sorafenib sensitivity, as p53-dependent apoptosis pathways are often modulated during acquired drug resistance in hepatocellular carcinoma. Moreover, the polyclonal format may better reflect the genetic heterogeneity observed in primary tumors.
This product is ideally applied in cancer biology and epigenetic regulation studies, including quantitative assessment of histone acetylation by ChIP-qPCR, apoptosis induction measured by TUNEL and caspase activation assays, and proliferation monitoring via MTT or BrdU incorporation. Western blotting and RT-qPCR can validate ING5 ablation and downstream target deregulation. The model supports drug sensitivity screening for agents such as sorafenib, and RNA-seq profiling to map ING5-dependent transcriptomic changes. For further technical details and ordering information, please contact Ascent Research.
