The HSD17B8 Knockout SK-HEP-1 Polyclonal Cells product supplies a CRISPR/Cas9-edited polyclonal population of the SK-HEP-1 human liver adenocarcinoma cell line. This bulk knockout model, generated through targeted disruption of the HSD17B8 gene, maintains population-level diversity and avoids single-cell clone artifacts. It is designed for researchers investigating the functional consequences of HSD17B8 loss in hepatic cancer.
SK-HEP-1 host cell line, originally isolated from the ascites of a patient with liver adenocarcinoma, exhibits an epithelial morphology and is a well-characterized model for hepatocellular carcinoma. It is extensively used in studies of cancer metabolism, invasion, and therapeutic resistance, making it an ideal background for gene-edited models of liver cancer.
HSD17B8 codes for a mitochondrial short-chain dehydrogenase/reductase essential in fatty acid elongation, where it catalyzes NADPH-dependent reduction of 3-ketoacyl-CoAs to 3-hydroxyacyl-CoAs. Independently, it reduces estrone to estradiol, thus linking lipid metabolism with steroid hormone biosynthesis. The enzyme is transcriptionally regulated by SREBP1c, PPAR??, and LXR??, and functionally cooperates with MECR and the mitochondrial fatty acid synthase complex. Downstream, it modulates levels of long-chain fatty acyl-CoAs, estradiol, testosterone, and other 3-hydroxyacyl-CoA intermediates. Consequently, HSD17B8 knockout is predicted to impair mitochondrial fatty acid synthesis and estrogen production, with broad metabolic repercussions.
Within the SK-HEP-1 liver cancer context, disruption of HSD17B8 offers a powerful system to probe the interplay between lipid reprogramming and hormone signaling. Given that both fatty acid elongation and estrogen activity are frequently dysregulated in hepatocellular carcinoma, this polyclonal knockout model can help elucidate how HSD17B8-mediated metabolic pathways contribute to tumorigenesis. It may also provide insights into related neurological disorders, including intellectual disability, peripheral neuropathy, and spasticity, where HSD17B8 mutations have been implicated.
Typical applications encompass metabolic flux studies, lipidomic profiling via mass spectrometry, and estradiol ELISA to quantify steroid hormone changes. The model supports drug sensitivity testing and functional genomics to identify synthetic lethal relationships or resistance mechanisms. Phenotypic characterization can be achieved through cell proliferation and apoptosis assays, mitochondrial fatty acid oxidation measurements, and standard expression confirmation by Western blotting and RT-qPCR. For additional technical information or to request custom modifications, please contact Ascent Research.
